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Flashcards in Boards Part 2 Deck (668):
1

Pacemaker for

• Third degree AV block or equivalent
(e.g., first degree AV block with LBBB and RBBB)
• Heart rate 3 seconds
• Sick sinus syndrome with symptoms (e.g., syncope)

2

Most common cause of tachycardia

re-entry

3

types of supraventricular tachycardia

• Sinus tachycardia
• Paroxysmal supraventricular tachycardia (PSVT)
• Sick sinus syndrome (SSS)
• Wolff-Parkinson-White/Lown-Ganong-Levine (WWW/LGL)
• Atrial flutter
• Atrial fibrillation

4

sinus tachycardia cause and tx

irritable SA node or atrial focus
Treat primary disorder (rehydrate, o2)

5

PSVT tx

Vagal manuevers (80%)
IV Adenosine or overdrive pacing

BB, CCB, Dig are preventitive

6

Short PR interval (<.12 sec)
Congenital accessory AV pathway

Tx for it

Wolff-Parkinson Whjite

Radiofrequency ablation is TOC

7

Sawtooth pattern seen in mitral stenosis, pericarditis and ARF

Atrial flutter

8

Irregularly irregluar rhythm

tx

Atrial fib

Rate control with BB or CCB
CVA proph with warfarin if chronic

9

> 3 cons PVCs

Vent Tachycardia

can be paired, multifocal or frequent

can lead to v fib

10

v tach etiology

• Usually due to ischemic heart disease and/or an acute myocardial infarction
• Prolonged QT syndrome
• Familial

11

* Typically presternal chest pressure radiating to the jaw and down the ulnar aspect of the
forearm
* Typically EXERTIONAL
* Stress related
* Cold temperatures
* Following a heavy meal

Tx too

Stable Angina

* Relieved with rest, O2, nitroglycerin

12

medical tx for CAD

* Treat risk factors
* (e.g., treat HBP, elevated LDL, DM, stop smoking)
* ASA 81 mg daily
* Sublingual nitroglycerin
* Beta blockers
* Calcium channel blockers - verapamil
* Long-acting nitrates transdermal nitroglycerin patches

13

interventional tx for CAD

* PTCA/stent
* Atherectomy
* CABG

14

* Progressively diminished exercise tolerance
* Increasing frequency and severity
* Relatively recent onset
(unstable angina with elevated biomarkers)

tx

Unstable Crescendo
Non-ST elevation MI

Immediate Hospitalization
O2, nitrates, BB, Anti-thrombotic tx

15

* Usually abrupt, severe and persistent
* EKG
* Biomarkers (CPK-MB; troponin-I; SGOT; LDH)

Tx

MI

* 9-1-1
* O2, nitroglycerin, and ASA to limit infarct size
* Early intervention/reperfusion
* tPA (tissue plasminogen activator)
* PTCA/stent, etc.
* Beta blockers: Acute and chronic benefit
* ACE inhibitors/statins: Chronic benefit/plaque stabilization

16

* Usually younger patient; at rest
* Usually few risk factors
* Occasional history of additional vasospastic disorders (e.g., migraine; Raynaud’s phenomenon)
* Focal spasm of an epicardial artery with ST elevation or spasm on coronary angiography

tx

Prinzmetal’s Angina

* Nitroglycerin
* Calcium channel blockers

17

* Asymptomatic MI
* May present with post MI complications (e.g., CHF)
* Frequent in diabetics
* “Autonomic dysfunction” prevents chest pain sensation during M

Silent MI

18

* Similar to angina, but not EXERTIONAL (It’s POSITIONAL)
* Often at night (supine position)
– Heartburn
– Pyrosis
– Dysphagia
* Often relieved with nitroglycerin and antacids
* Often midepigastric tenderness on Px

GERD

19

Causes of Chest Wall Pain

* Usually some form of trauma/strain
– ? Severe coughing paroxysm
– ? Heavy lifting, etc.
* Often pleuritic

20

* Pain may radiate to left shoulder
* Often relieved with sitting up and leaning forward
* Physical exam:
– ? Pericardial friction rub
– ? Pulses paradoxus (decrease in BP with inspiration)

Pericarditis

21

* Severe, abrupt, radiating to the back
* Physical exam:
– ? Loss of lower extremity pulses
– Possible murmur of AI

Chest Pain Secondary to Aortic Dissection

22

Chest Pain
* Variable and usually atypical pattern
* Often associated with a history of anxiety and depression
* Often precipitated by situational factors
* Diagnosis by exclusion

Psychophysiological Chest Pain

23

HTN goals for blacks w/ and w/out organ damage

135/85 if none
130/80 is evidence

24

HTN definitions

• Normal BP 120.
• Isolated systolic hypertension: Systolic BP >139, normal diastolic BP

25

aldoseterone does what

Causes Renal Na retention to increase blood volume

26

Hypertension with not direct cause

Risk factors
– Genetics
– Sodium consumption
– Obesity
– Alcohol abuse
– Type 2 diabetes
– Type “A” personality

Essential HTN

27

HTN worsened with sodium consumption

types and treatment

Salt Sensitive

– Low renin essential hypertension
• ? Excess production of unknown mineralocorticoid which does not waste potassium
• Dietary sodium restriction helpful
• Diuretics helpful
– Normal / high renin (nonmodulating) essential hypertension
• Possible renal defect (inadequate sodium excretion)
• 25-30% of essential hypertension
• ACE inhibitors helpful
– High renin essential hypertension
• Probably due to increased catecholamine activity
• Beta blockers helpful
• Renin blockers helpful

28

2ndry HTN causes

• Renal hypertension
– Renovascular hypertension
– Primary renal disease
• Endocrine hypertension
– Aldosteronism (usually primary aldosteronism)
– Cushing’s disease
– Pheochromocytoma
– Contraceptive-induced (estrogen stimulates hepatic angiotensinogen production)
– Hyper- or hypothyroidism
– Hyperparathyroidism
• Aortic coarctation
• Obstructive sleep apnea

29

HTN with hypokalemia tx

Spironolactone

30

– Rapidly escalating hypertension
– Borderline elevated / rising creatinine
– Abrupt creatinine rise following ACE inhibitors
– History of diabetes, dyslipidemia, smoking, ASCVD

dx and tx

Renovascular HTN

• Diagnosis
– Renal artery ultrasonography; MRA; spiral CT scan
– Renal artery angiography +/- renal vein renins
• Treatment
– Ideally, stenting

31

– Hypokalemia
• ACTH; renal artery ultrasonography
– Plasma aldosterone concentration and plasma renin activity levels
• PAC > 20 and PAC/PRA > 30 highly suggestive
– Imaging: CT/MRI

Hyperaldosteronism

32

– Symptoms usually include a severe headache, vomiting, visual disturbances, CNS findings (paresis, convulsions, lethargy, coma) cardiac decompensation and oliguria
– Diastolic BP generally >130 mm of mercury, papilledema, retinal hemorrhages

Malignant HTN

furosemide IV 40mg
and either nitroprusside 0.25mcg/kg/mm or nitroglycerin 5mcg/min

Caustion do not lower diastolic BP to

33

– No evidence of end organ damage (e.g., normal CMP or chronic abnormalities, normal UA,
troponin I, no acute EKG changes, symmetrical pulses, no papilledema or retinal hemorrhages:

Severe HTN

Clonidine 0.1 every 2-3h

34

– Pregnancy with hypertension, proteinuria and hyperreflexia; may present with convulsions

tx

Eclampsia

mg sulfate 4gIV for convulsions
Hydralazine 5-10 mg IV for HTN (to d < 95)
Consider urgent delivery

35

HR that compromise perfusion

Generally HR 140 compromises perfusion due to inadequate time for sufficient preload

36

Physiologic / Cardiac Compensation for CHF

Renal:
– Increased sodium and water retention with renin angiotensin system activation to increase
blood pressure for perfusion and to augment preload
Autonomic nervous system:
– Increased heart rate to increase cardiac output
Cardiac:
– Muscular hypertrophy
– Maladaptive cellular remodeling / fibrosis

37

systolic CHF and Diastolic CHF

Systolic CHF
– Primarily contractility and/or afterload problem (e.g., acute hypoxemia)
Diastolic CHF
– Primarily preload problem (e.g., “stiff” fibrotic ventricle)
NOT to be confused with right heart failure and left heart failure

38

CHF symptoms

– Primarily dyspnea on exertion
– Orthopnea / paroxysmal nocturnal dyspnea
Increased pulmonary capillary pressure due to fluid shift from the extremities when supine;
possible impaired apical pulmonary arteriolar oxygenation due to pulmonary effusion
– Dependent edema
– Cheyne-Stokes’ respirations
Primarily CNS symptom likely

39

CHF physical findings

– Bibasilar inspiratory rales
– Cardiomegaly / laterally displaced PMI; S3gallop
– Dependent edema / pleural effusions / ascites
– Hepatomegaly / positive HJR / JVP >8 cm (major criteria: >16 cm) / jaundice

40

Lab for CHF

Blood work: CBC, CMP, TSH, UA, NT pro-BNP (byproduct of stretching myocytes)

41

tx for CHF

Diuretics
Sodium restriction
BB
ACEi
Digoxin
Vasodilators

42

RV failure usually due to increased
RV afterload / pulmonary vascular resistance
– Usually due to COPD and increased pulmonary capillary pressure from hyperinflation
– Interstitial pulmonary disease / fibrosis
– Pulmonary vasoconstriction
(e.g., hypoxemia; altitude sickness)
SOB, light head, palpitations, Chest pain, blue skin

Cor Pulmonale

43

50% mortality in 60 minutes from acute pulmonary embolism
Usually due to acute pulmonary embolism
– Possible high altitude pulmonary edema
(HAPE); acute pulmonary inhalation injury, etc.
Physical findings:
– Right heart failure signs; S4 gallop

tx

Acute cor pulmonale

O2 diuretics, treat underlying cause

44

Pulmonary Hypertension Treatment

Treat underlying cause
Oxygen
Vasodilators
– Calcium channel blockers; ? sildenafil (Viagra)

45

Classifications of cardiomyopathies

* Dilated
* Hypertrophic
* Restrictive

46

* Signs and symptoms of CHF
* Usually die within three years from onset of symptoms
* Rule out ischemic heart disease; work-up like CHF

Dilated Cardiomyopathy

47

* Second most common cause of CHF after ischemic heart disease
* Reversible if alcohol consumption is discontinued before advanced disease
* “Holiday heart syndrome”
* Arrhythmias (usually AF) after a binge

Alcoholic Cardiomyopathy

48

* First symptom may be sudden death with strenuous activity (esp in kids and young adults)
* May be slowly progressive and present as atrial fibrillation or CHF in older patients
* Physical findings
Include late systolic ejection murmur along the LLSB radiating to the apex
* EKG findings
LVH and often diffuse broad Q waves from increased muscle mass opposite the
electrode; possible LAE; possible atrial fibrillation
* Echocardiogram: Diagnostic
Septal hypertrophy, left ventricular hypertrophy and systolic prolapse of the anterior
mitral valve leaflet

and Tx

Hypertrophic Cardiomyopathy

BB or diltiazim (opposite of CHF)

49

* Diastolic CHF due to infiltrative disorders such as amyloidosis and hemachromatosis;
idiopathic; familial endomyocardial fibrosis
* Signs and symptoms of CHF
* Treatment
* Treat diastolic CHF; arrhythmias

Restrictive CM

50

* Cardiac muscle inflammation
* Usually infection (e.g. viral, bacterial, lyme carditis; Chagas’ disease
* Rarely autoimmune (giant cell myocarditis)
* Symptoms and signs of CHF
* Treatment
* Treat systolic CHF, arrhythmias, underlying disorder

Myocarditis

51

from multiple etiologies (e.g., infection, acute MI, uremia, trauma /
Dressler’s syndrome, metastatic disease, drugs like INH)
* Symptoms
* Usually chest pain referred to the back with dyspnea
* Usually relieved with sitting and leaning forward
* Physical findings
* Pericardial friction rub; pulses paradoxus
* EKG findings: Often diminished QRS amplitude

and Tx

Pericarditis

Treat underlying cause
Pericardiocentesis: pericardial window

52

Opening snap rumpble
augmented with exercise
right CHF findings
EKG: LAE
Can have A fib

Mitral stenosis

53

• Increased left atrial pressure with symptoms of pulmonary hypertension and cor
pulmonale
• Regurgitated LV preload and symptoms of reduced cardiac output (e.g., dyspnea on exertion)
– Physical findings
• S3and occasional S4gallop
• Holosystolic murmur at the apex radiating to the left axilla
– EKG findings: LAE; +/- RAE; +/- LVH
– Echocardiogram: Diagnostic

Mitral regurgitation

54

– Symptoms:
• Usually none
• Occasional PSVT due to LA “stretch”
– Physical findings:
• Midsystolic “click–murmur” augmented with isometrics and valsalva (reduced LV preload and
leaflet angle with increased papillary muscle “slack”)
– EKG: Usually normal
– Echocardiogram: Diagnostic

Mitral valve prolapse

• SBE prophylaxis if MR present
• Beta blockers for PSVT

55

Angina
Exertional Syncope (hypotension from vasodilation and exercising muscles with compromised cardiac output)
Pulses parvus et tardus
Reduced S1-S2 interval and possible paradoxical splitting of S2
S4
Systolic ejection murmur

Aortic stenosis

56

often asymptomatic
• “Water hammer” pulse with widened pulse pressure (e.g., 140/60); “Quinke’s pulse” with
gentle pressure on nail bed; markedly augmented PMI with lateral displacement
(e.g., head bobbing/”bed spring” pulse)
• Diastolic decrescendo murmur
EKG: LVH

Aortic Regurgitation

57

SBE prophylaxis indications

– Previous history of SBE; prosthetic heart valves; prosthetic material used for cardiac valve
repair; unrepaired cyanotic congenital heart disease; repaired congenital heart disease with
residual defects at the site of a prosthetic device; cardiac valvular disease in a transplanted heart
• Treatment prior to dental procedures:
– Amoxicillin 2 gm orally one hour before procedure
– Clarithromycin 500 mg one hour before procedure if penicillin allergic
• Treatment prior to procedures on infected skin or musculoskeletal tissue
– Infections often polymicrobial but only staph and beta hemolytic strep bacteremia are likely to
cause endocarditis
– Treat as above pending culture results and consider the addition of TMP SMX DS if suspicious
of MRSA

58

Categories of hyperlipoproteinemia

• Type II-a hyperlipoproteinemia
– Elevated cholesterol; normal triglycerides
• Type II-b hyperlipoproteinemia
– Elevated cholesterol; elevated triglycerides
• Usually seen with type 2 diabetes

59

Acquired dyslipidemia

obesity
Type 2 DM
Hypothyroidism
Liver Disease
Renal Disease

60

Treatment goals for risk factors

0 – 2 <70

61

Risk factors for LDL elevation

– Cigarette smoking
– Hypertension (BP 140/90 mmHg or on antihypertensive medication)
– Low HDL cholesterol [<65 years
– Age (men 45 years; women 55 years)
– Lifestyle risk factors
• Obesity (BMI 30 kg/m2)
• Physical inactivity
• Atherogenic diet
– Emerging risk factors
• Lipoprotein(a)
• Homocysteine
• Prothrombotic factors
• Proinflammatory factors
• Impaired fasting glucose
• Subclinical atherogenesis

62

tx for elevated cholesterol

• Nonpharmacologic treatment
– Smoking cessation – increases HDL
– Weight control – decreases LDL
– Exercise – increases HDL
– Treatment of underlying problems such as diabetes and hypothyroidism
– Dietary treatment
• Low saturated fat
• No dietary sweets

63

combo therapy for elevated cholesterol beware of what combo and why

Beware of statin/fibrate combination (myositis; rhabdomyolysis; elevated CPK)

64

meds for cholesterol and what they target

LDL only - Statin
LDL, HDL, TG - Niacin
TG only - Fibric acid derivatives
LDL - Ezetimibe

65

Big QRS
Compensatory pause

PVC

66

PVC falls on what wave cause vent tachycardia

T wave

67

torsade de pointes (Vent fib with twisting axis) cause

Congential QT syndrome

68

Long PR consistently prolonged

1 deg AV block

69

PR interval consistently increases in successive cycles
lack of QRS

Wenkenbach 2 AV block

70

2:1 P to QRS

Mobitz 2 AV block

71

3:1 P to QRS

Mobitz 3 AV block

72

PR interval not the same
Normal QRS

3 AV block

73

bunny ears

Bundle branch block

74

Diphasic P wave

RAH or LAH

75

Large R wave in V1

RVH

76

Large S wave in V1
Large R wave in V5

LVH

77

t wave inversion

ischemia

78

ST elevation

Injury

79

ST depression

subendocardial infarction
positive stress test
digitalis

80

significant q waves

infarctions

81

infarct leads

sig q waves

I and AVL = Lateral
V1, V2, V3, V4 = Anterior
II, III, AVF = inferior

82

U waves

hypokalemia

83

A-a gradient

• Difference between alveolar O2and arterial O2
• For arterial PaO2of 80
97-80 = 17 A-a gradient of 17
• Normal A-a gradient is 7-14 on room air

84

Arterial Blood Gas Analysis PaO2: Measure of Oxygenation
Arterial Blood Gas Analysis PaCO2: Measure of

Ventilation

85

Pulmonary Function Testing
Major Types of Tests

• Spirometry (pre and post dilator)
• Forced inspiratory maneuvers
• Lung volumes
• Diffusing capacity
• Maximal respiratory pressures
• Pulse oximetry – rest and exercise

86

Major Types of Pulmonary Disease Identified by PFTs

• Obstructive lung diseases
- Asthma, COPD, CF
• Restrictive lung disease
- Pulmonary fibrosis, sarcoidosis, neuromuscular disease, pulmonary edema
• Mixed pattern

87

PFTs in Obstructive Lung Disease

• Spirometry
- Low FEV1/FVC (12%) in asthma

88

PFTs in Restrictive Lung Disease

• Spirometry: Reduced FVC but normal or even increased FEV1/FVC ratio (>70%)
• Lung volumes: Decreased total lung capacity (<80% predicted)
• Diffusing capacity: Usually decreased
Use of Pulse Oximetry in Clinic Setting
• Measure oxygen saturation at rest
• Monitor oxygen saturation . . .
- With exercise
- With sleep
- During procedures

89

Hyper-responsiveness – response to triggers->Obstruction – usually fully reversible->
Symptoms – cough, wheeze, dyspnea, dec breath sounds
- Airway bronchspasm
- Airway inflammation and mucus
• Bronchospasm
- Airway narrowing
- Usually worse at night
- Triggers: Pollen, drugs, dust, exercise, smoke exercise, cold, stress, colds/flu

Asthma

90

Assessment of bronchospasm of Asthma

• Spirometry: FEV1
• Peak flow meter
• Use of bronchodilators
• Symptoms
- Particularly nighttime awakenings

91

FEV1/FVC improves with dilator

Asthma

92

Signs of poor control of asthma

(rule of 2s)
- Use “rescue” meds >2 times/week
- Nighttime awakening due to breathing >2 times/month

93

• Defines a severe asthmatic episode that is not responsive to repeated treatments with usual
inhaled medications

Status Asthmaticus

94

Treatment of Asthma

• Mild disease
- Avoid triggers
- Use of short-acting inhaler as needed
• Moderate-severe disease
- Inhaled corticosteroids
- Inhaled long-acting bronchodilator
- Leukotriene receptor antagonist
Especially for aspirin sensitive asthma
- Oral steroids
- Anti-IgE therapy (Xolair - IgE antagonist injection every 2 weeks)

95

best way to improve COPD

smoking cessation

96

Low flattented diaphragm
increased AP diameter
Air trapping

COPD

97

Therapy in COPD

• Smoking Cessation
• Drug Therapy
--B2 agonists, anticholinergics
• Oxygen Therapy
• Exercise/Nutrition
• Lung Volume Reduction
• Lung Transplantation

98

• Respiratory manifestations
- Persistent, productive cough
- Airflow obstruction
- Bronchiectasis-dilated airways
• Physical findings
- Wheezing
- Clubbing of digits
• Sweat chloride: Sweat chloride level of >60 meq/L
- Pancreatic insufficiency with malabsorption
• Infertility

Cystic Fibrosis

99

Restrictive lung diseases

• Interstitial Lung Disease
• Neuromuscular Disease
• Severe Obesity
• Chest Wall/Spine Deformity
• Pleural Disease

100

interstitial lung dieseases causes

• Drugs
- Chemotherapy, amiodaronenitrofurantoin
• Toxic Dusts
- Asbestos, silica
• Hypersensitivity Pneumonitis
- Organic dusts
Interstitial Lung Disease:Associated with Systemic Disease
• Rheumatoid Arthritis
• Scleroderma
• Systemic Lupus Erythematosis
Interstitial Lung Disease:Idiopathic
• Sarcoidosis
• Idiopathic Pulmonary Fibrosis

101

• Shortness of breath
- Particularly with exercise
• Cough
- Usually non-productive
• Radiographic
- Diffuse linear (reticular) or nodular markings in lung parenchyma
• PFTs
- Reduced lung volumes
- Reduced diffusing capacity (usually)

Features of ILD

102

• Military Exposure (ships/tanks)
• Ship-Building
• Boiler worker
• Electrician
• Brake Repair
• Construction
• Building Remodeling

ILD: Asbestos

103

• Mining
• Sand-blasting
• Metal working
• Glass workers

ILD:Silica

104

Drug induced ILD

• Cancer patients
- Many chemotherapeutic agents cause ILD, some not until years later
• Cardiac patients
- Amiodarone: Used for arrhythmias
• Arthritis patients: Methotrexate
• Urinary tract infections: Nitrofurantoin

105

Hypersensitivity Pneumonitis ILD

exposure to organic dusts
agriculture, moldy hay

106

most common cause of reduction in lung volumes, particularly total lung capacity
• Diffusing Capacity (DLco) is generally not affected

Obesity and restrictive Changes in PFTs

107

Idiopathic Interstitial Lung Disease
- Increased frequency in African-American
• Clinical Presentation
- Cough, Short of Breath (Lung involvement in 95% of Sarcoid pts)
- Skin Rash
Erythema Nodosum
- Eye symptoms (iritis)
- Neurologic symptoms
- Joint pains
-“Potato” hilar adenopathy
-Facial sarcoid granulomatous nodules
- “Lupus pernio” - facial sarcoid granulomatous plaque

Sarcoidosis

108

Sarcoid Dx

• Radiographic
- Hilar/Mediastinal Adenopathy
- Pulmonary Infiltrates
• Pathologic
- Granulomas: Non-caseating

109

• Increased prevalence in older ages
• Progressive fibrosis of the lungs
• Mean survival is only 3-4 years
• Clinical Features
- Crackles in Chest
- Clubbing of Digits is Common
• Exclude Other Causes of Pulmonary Fibrosis
• Characteristic Features on CT: may make diagnosis
Interstitial fibrosis with adjacent normal lung tissue, extensive honeycombing

Idiopathic pulmonary fibrosis

110

Treatment of ILD

• Known Causes
- Avoid/eliminate exposure
- Corticosteroids
• Sarcoidosis
- Corticosteroids
- Methotrexate
• Idiopathic Pulmonary Fibrosis
- No proven therapy, ? Pirfenidone
- Transplant

111

ARF types

• Hypoxemic Respiratory Failure
- Low Oxygen Level
• Hypercapnic Respiratory Failure
- High Carbon Dioxide Level

112

• Acute Lung Injury: Milder injury to lung
• Acute Respiratory Distress Syndrome (ARDS):
Severe disorder where oxygenation is markedly abnormal (A-a gradient >200)
- Approx 150,000 cases/year mortality 35-50%
• Can be caused by direct injury to lung
- Aspiration gastric contents
- Toxic inhalation – smoke
- Severe pneumonia
- Exposure to drugs toxic to lungs
• Systemic Injury
- Shock/trauma, sepsis, drug overdose, pancreatitis, burn injury

Hypoxemic Respiratory Failure

113

Pathophysiology of Hypoxemic Respiratory Failure (ARDS)

• Alveoli fill with fluid, become unstable and collapse
• Collapsed alveoli results in V = 0 which is definition of shunt
• Characteristic feature of ARDS is low oxygen that does not respond to supplemental oxygen
(A-a gradient >200)

114

Treatment of ARDS

• Ventilation: usually an endotracheal tube, occasionally by mask
• Positive pressure throughout ventilation
• Positive end-expiratory pressure (PEEP)
- Supplemental oxygen
- IV fluids and nutrition
- Antibiotics if needed

115

Cause of death in Hypoxemic Resp failure

infectious complications

116

• May present as drop in SaO2 since increase in PaCO2 will cause decrease in PaO2
• Diagnosed by arterial blood gas demonstrating increased PaCO2
• If acute, patient will have respiratory acidosis (pH 7.2

Hypercapnic Respiratory Failure

117

some causes of hypercapnic resp failure

• Advanced COPD
- Severe COPD Exacerbation
• Severe Asthma
- Status Asthmaticus
• Neuromuscular Disease
• Hypoventilation
- Trauma, stroke, drug effect, over-sedation

118

most common presenting symptom of lung cancer

cough

119

syptoms of lung cancer

- cough
- Hemoptysis
- Wheeze, shortness of breath
- Dysphagia
- Weight loss
- Chest discomfort
- Signs of metastatic disease

120

types of lung cancer

• Adenocarcinoma
• Squamous Cell Carcinoma
• Small Cell Carcinoma (“oat cell”)
• Large Cell Carcinoma
• Bronchoalveolar Cell Carcinoma (BAC) type of adeno-ca that occurs as often in nonsmokers as
in smokers

121

Staging of Lung Cancer

• Stage 1
- Small (, 3 cm) disease without involvement of any lymph nodes (N0)
• Stage 2
- Larger disease, possible hilar node involvement (N1)
• Stage 3
- Mediastinal lymph node involvement (N2)
• Stage 4
- Metastatic disease (M)

122

Therapy of lung cancer

• For Non-small Cell Lung Cancer, surgery is the only therapy that offers a significant chance at
long-term survival (>5 years)
• Surgery is possible in Stage 1 disease and in selected patients with Stage 2 disease
• Surgery is generally not recommended except in experimental trials in Stage 3 disease

123

Methods to stage lung cancer

CT scan
PET scan

124

ddx of lung nodule

• Granuloma
- Usually due to fungal infection
- Most often Coccidoidomycosis in Az
• Lung Neoplasm
- Primary or metastatic
• Other unusual causes
- Benign tumors including hamartoma, fibroma, etc.

125

what if you see a neoplasm in the airways

neoplasm (not cocci)

126

early diagnosis of lung cancer

Routine CT scans

127

lung cancer metastases sites

bone
brain
liver
adrenal glands

128

cancer of surface of lung (pleura) often related to asbestos exposure

Mesothelioma

129

metastatic disease to lungs

Breast
Colon
Kidney
Melanoma

130

common cold causes and tx

rhinovirus
no antibiotics
treat with tylenol, etcc

131

• Constitutional symptoms are more prominent than in cold
- Fever, malaise, myalgias
- Often seasonal
• Treatable within first 2 days
- Oseltamvir (Tamiflu): 75 mg bid for 5 days
• Influenza prophylaxis
- Oseltamvir (Tamiflu): 75 mg once daily for 6 days
- Flu shots

Influenza

132

• Usually viral
• 15% Strep
- Exudate with fever and lymphadenopathy

tx

Acute pharyngitis

Penicillin or erythromycin

133

* Usually posterior cervical adenopathy, a dull white exudate and possible hepatomegaly or
splenomegaly
* Rash if given amoxicillin

Mononucelosis

Penicillin or erythromycin

134

• Primarily results from sinus ostial obstruction (“ostiomeatal complex” obstruction)
-

Acute sinusitis

Narrow spectrum antibiotics
Amoxicillin or Bactrim

135

sinus obstruction > 12 weeks cause

bacterial or fungal

get sinus CT

136

Achy ear
- Often due to pseudomonas aeruginosa and occasionally staph aureus
- Generally treated with ciprofloxacin– HC drops topically and debridement; occasionally with
systemic antibiotics
- Avoid Q-tips

Otitis externa (Swimmer's ear)

137

usually bacterial following a viral URI
- S. pneumoniae; H. influenza; M. catarrhalis
- RX: amoxicillin although 1/3 resistant; treatment debatable

otitis media

138

tx for serous otitis media


- Consider antibiotics and/or myringotomy tubes if significant hearing loss and effusion > 3 mo

139

- Potentially fatal
- Dx: Lateral neck films ; cherry red epiglottis with fiberoptic rhino-laryngoscopy

acute epiglottiis

ampicillin/sulbactam or 2/3 cephalosporin
maybe hospitalization

140

usually viral
• Characterized by cough, usually with sputum production
• The absence of abnormalities on chest radiography distinguishes from pneumonia

acute bronchitis

141

severe bronchitis symptoms

- Increased amount of sputum
- Change in color of sputum
- Increased shortness of breath
• Treat severe bronchitis with antibiotics for 7-10 days
- azithromycin or levofloxacin
• May need to treat associated bronchospasm (e.g., albuterol; steroids)

142

• Primary symptom is chest pain, worse with inspiration
• Usually viral
• Treat symptomatically
- Non-steroidal anti-inflammatory drugs

Pleurisy

143

URI and LRI
What are LRIs

pneumonias

144

• Infection that extends beyond airways into pulmonary parenchyma (lobe, lobules)
• Characterized by more change in gas exchange (shortness of breath), and presence of abnormal
findings on chest radiograph or CT scan
• Associated morbidity/mortality is much higher than bronchitis

pneumonia

145

symptoms of pnuemonia

• Cough, usually productive
• Fever, chills
• Dyspnea
• Malaise
• ? Confusion
• Symptoms may vary from severe to absent

146

Physical Findings in Pneumonia

• Fever and tachycardia
• Tachypnea (RR > 20)
• Auscultation of chest
- Common: Crackles (“rales”)

147

Types of pneumonia

• Bacteria (most often)
- Gram positive: Strep pneumonia,
- Gram negative: Klebsiella, pseudomonas,
• Fungal
- Coccidioidomycosis (Valley Fever), histoplasmosis, blastomycosis, aspergillis
• Mycobacteria
- Mycobacterium tuberculosis, mycobacterium avium-intracellulare
• Viral
- Respiratory syncytial virus, adenovirus, influenza

148

Clinical Signs of Severe Pneumonia

• Hypoxemia
- SaO2 < 92%
• Tachycardia
• Hypotension
• Altered mental status
- Obtundation
- Confusion

149

diagnosis of pnuemonia

• Primarily from history and physical exam
• Chest x-ray / chest CT scan
• Sputum Gram stain and culture
- ? Acid fast bacilli stain, KOH, fungal cultures, mycobacterial cultures, etc.
• Blood cultures
• Serologic testing
- e.g., coccidiomycosis antibody titers

150

walkling pneumonia

- Some organisms (mycoplasma or chlamydia) may cause mild symptoms

151

tx for pneumonia

• More severely ill pt, initial empiric coverage w/multiple antibiotics for a variety of pathogens
- e.g., ceftriaxone 2 g IV daily with levofloxacin 750 mg orally daily
• In immuno-suppressed patients, consider bronchoscopy with lavage (bronchoalveolar lavage)
to evaluate for atypical pathogens
• Usual outpatient treatment: Empiric macrolide (e.g., azithromycin) for mild sy mptoms or
quinolone (e.g. levofloxacin) if moderate symptoms

152

• May present as community-acquired pneumonia; possible history of soil dust exposure (e.g.,
lives in a developing suburban subdivision)
• Often causes a cavity to form within the lung
• Can be associated with severe constitutional symptoms
• Diagnosis: Serologic test or culturebof organisms
Miliary pattern on CXR
eosinophilia

tx

coccidiomycosis

• Most cases will resolve without any treatment
• Can use Diflucan (fluconazole) 200 mg twice daily for therapy
• In severe cases, may use Amphotericin B by IV administration

153

- Evidence of tuberculosis organisms multiplying in pulmonary or extra-pulmonary site
- Often infectious to others

active TB

154

- Cough and minor symptoms for 2-4 weeks and central infiltrates on chest x-ray
- Usually not infectious

Primary TB

155

- “reactivated” tuberculosis; symptoms may be similar to pneumonia with peripheral and apical
chest x-ray infiltrates
- Infectious

2ry TB

156

• Cough
• Weight loss
• Fatigue
• Fever and night sweats
• Sputum production
• Hemoptysis (usually late in disease)
• Dyspnea

TB symptoms

157

reactivation TB usually involves what

upper lobes
cavity will form

158

• Patients with a positive Tb skin test, but no evidence of active tuberculosis have what is
termed

latent tb

159

Approach to Patient with Suspected Latent or Active Disease

• Latent disease: Tb skin testing (PPD-“purified protein derivative” or “Mantoux” testing)
- mandatory in certain occupations
• Suspect active disease
- Isolate the patient
- Sputum AFB smear and AFB culture x 3
- Occasionally will need bronchoscopy
• If find active disease: Skin test all contacts

160

TB test interpretation

• Positive
- ≥ 10 mm induration
- ≥ 5 mm if:
* HIV
* Immunosuppressed
* Recent close contact
* Radiographic evidence of old TB

161

Latent TB tx

isoniazid 9 months with B-6

162

Active TB tx

isoniazid plus B6
Ethambutol
Rifampin
Pyrazinamide

163

DVT study

Duplex ultrasound

164

1. Pleuritic pain or hemoptysis 65%
2. Isolated dyspnea 22%
3. Circulatory collapse 8%
No dyspnea is present 27%

Tachypnea (>20) 70%
Tachycardia (>100) 43%
Crackles (rales) 53%

PE

165

Interventions to Reduce Risk of DVT/PE

• Early ambulation after surgery
• Avoid prolonged immobilization
• Compressive stocking or mechanical compressing devices
• Prophylactic treatment with low-dose heparin in high-risk patients
- e.g., low-dose heparin or Lovenox postoperatively then 4-6 weeks of Coumadin following a
total knee arthroplasty or total hip arthroplasty

166

Diagnosis of PE

Spiral CT! (contrast enhanced)
VQ scan
D-dimer (sensitive to rule out)

167

Treatment of Pulmonary Embolism

• Initial therapy: Heparin
• In unstable patient – may consider thrombolytic therapy or surgical embolectomy
• Long-term therapy: Warfarin (Coumadin)
- 1stepisode: 6 months of therapy
- 2ndepisode: Lifelong
- Predisposing factor: Lifelong

168

MICROCYTIC ANEMIAS

• IDA
• ACD
• Hemoglobinopathy (eg THAL)
• Sideroblastic anemias (lead poisoning)

169

• Most common anemia
• Most common cause: blood loss
• Occasionally malabsorption from:
– Gastric surgery
– Malabsorptive disorders
High Transferring
Low serum Iron
Low Ferritin

Iron Def Anemia

dietary iron - meat
oral iron

170

• Characterized by:
– ↓Fe
– ↑↑Ferritin
– ↓ EPO
• Develops in:
– Chronic infections
– Chronic inflammatory disease
– Neoplastic disease

anemia of chronic disease

171

Macrocytic = megalo & non-megalo

Name causes of megaloblastic (oval) anemias

• B12/Folate def
• Drugs:
– dilantin/OC
– hydrea/methotrexate
• Some marrow disorders

172

– ↑ RBC Mass
– Normal O2
– Splenomegaly
– Increased: WBC / PLTS / B12 / LAP score
– JAK-2 Mutation
– Bone Marrow Hypercellularity

Primary Polycythemia vera

173

polycthemia vera tx

– Phlebotomy (do it until hct under 45)
• H/H < 15/45 – decreases thrombotic risk
– Hydroxyurea

174

Anemia from reduced RBC survival (<100 days)
Bone marrow unable to replace RBCs
Etiologies
Immune - Coomb’s Positive
Non-immune - Coomb’s Negative

Hemolytic anemia

175

– Rapid pallor / anemia
– Jaundice
– Splenomegaly
– Increase:
MCV - macrocytosis
• Reticulocytes
– IMMUNE: (+) Direct anti-globulin test(Coomb’s)
– History of pigmented(Bilirubin) gallstones

hemolytic anemia

176

HEMOLYTIC ANEMIA – ACQUIRED ETIOLOGIES
IMMUNE (Coomb’s +)

 Autoimmune Hemolytic anemia(AIHA)
 Warm: Idiopathic & CLL
 Cold: Idiopathic & Mycoplasma
 Alloimmune: Transfusion
 Drug-induced

177

– Antibody or complement on RBC (looking for abs on RBC)
– Diagnosis of:
• AIHA
• Hemolytic transfusion reaction

direct coombs

178

– ATB in SERUM NOT bound to RBC
– Patient serum & Donor RBC
– The screen in: “type & screen”
– In autoimmune hemolysis
• both DAT & IAT may be (+)
• ATB may be in SERUM & ON RBC

indirect coombs

179

– Auto-ATB against RBCs
– Warm & Cold Auto-ATB

AIHA

180

 Any Age
 Usually IgG
 Variable anemia
Etiologies:
 65% - Idiopathic
 25% - CLL
 20% - NHL
 Other – Meds
Clinical
 Anemia
 Jaundice
 Splenomegaly

warm auto ATB

181

– IgM
– Etiologies:
• Idiopathic
• Mycoplasma
• Lymphoma
• Mononucleosis
– Clinical
• Acrocyanosis at cold temperatures
• Jaundice
• Splenomegaly

cold auto atb

182

acquired clonal stem cell disease
– Cell membrane anchor defect
– Hemolytic anemia
– Screen using: CD55 and CD59

and treatment

Paroxysmal Nocturnal Hemoglobinuria

Elulizumab
-binds complement C5

183

Inherited hemolytic blood disease resulting from a mutation in the alpha globin gene
• Normal HGB = “A1”
• Hemoglobin “S”

Sickle Cell Disease

184

Sickle Cell Types

– “Trait” = Heterozygous = A>S
• 8% of Aas
• Malaria protection
– “Anemia” = Homozygous = SS
• sickle cells in PS
– Sickle cell – Hemoglobin C = “SC”
• fewer sickle cells - more Target / Spherocytes
– Sickle-Thal

185

Vaso-occlusive disease of sickle cell

– SC accumulate in any vascular bed
– Infarction of Marrow/Spleen/Kidney
– Painful crises in long bones
• MOST COMMON PRESENTATION

186

sickle cell skeletal presentation

• Marrow hyperplasia=osteopenia=fractures
• “Hair-on-end” on skull
• Marrow infarction = osteonecrosis
• Dactylitis
• Osteonecrosis
• Bossing

187

– 8% of African Americans
– A always > S
– Under physiologic conditions no vaso-occlusion
– Carriers have normal life expectancy
– Compared to the general population:
• Same risk for:
– Heart disease
– Stroke
– Anesthetic agents

sickle cell trait

188

– Imbalanced globin chain synthesis:
• Ineffective hematopoiesis
• Defective Hgb production
• Hemolysis
• Variable anemia

types and explian

• Beta Thalassemia
– Beta reduce or absent
– Alpha excess
• Alpha Thalassemia
– Alpha reduced or absent
– Beta excess
• Quantitative NOT Qualitative disorder

189

heinz bodies

excess alpha chains

190

– Heterozygous carrier
– Usually no clinical symptoms
– Asymptomatic Splenomegaly 20%
– CBC/peripheral smear
• Mild anemia(Hct>30)
• MCV

B-Thal Minor

191

• Anemia later and milder than major
• Requires less transfusion
• Retarded growth/development
• Skeletal deformity
– EPO increases marrow expansion
– Deformities of skull / long bones
– Pathologic fractures
• Splenomegaly
• Milder forms:
– Asymptomatic & xfusion independent
– Hgb 10-12

B thal Intermedia

192

• Homozygous “Cooley’s Anemia”
• Symptoms begin at 4-6 months
• Clinical:
– Gallstones
– Leg ulcers
– Skeletal disease
– Anemia
Laboratory features
• Microcytic anemia
• Target cells / Tear drop cells / Basophilic stippling / NRBCs

B thal Major

193

Pathophysiology Alpha Thalassemia

– 4 copies of α globin gene
• 2 copies each Chr. 16
– 1 Deletion = AT Minima
– 2 Deletions = AT minor
• TRANS: A/- A/-• CIS: AA / --– 3 Deletions = Hgb H Disease
– 4 Deletions = Hgb Bart’s

194

– Silent carrier = (α - / α α)
– Trait
• Similar to β Thal trait
• Mild heme changes
• No clinical abnormality

a Thal (silent carrier)

195

• Mod-severe hemolytic anemia – hypo/micro –retic counts to 15%
• HSM / Gallstones / Leg ulcers
• RBCs contain Hgb H precipitates

– Hgb H Disease (α - / - -)

196

– Hgb Bart’s (- - / - -) (γ4) =

incompatible with life

197

other names for myelodysplastic syndromes

– Refractory anemia
• No improvement with Fe / B12 / Folate
– Pre-Leukemia
– Senile anemia

198

Ringed sideroblasts

myelodysplasia

199

• Heritable mutation = RUNX-1
• Tobacco
• Ionizing Radiation
– Highest rate of progression to AL – 75%
– Low response to treatment
– Median survival ~ 9 MOS.
– Chromosome abnormalities:
• -5 / -7 = Alkylating Agents
• 11 = Topo-II inhibitors
Clinical:
– Signs / symptoms usually from cytopenias
• Anemia
• Infection
• Bleeding
– Usually absent:
• Lymphadenopathy
• Hepatosplenomegaly
Peripheral smear:
• Macrocytosis
• Hypolobar neutrophils
– (Pseudo Pelger-Huet)
• Circulating micromegakaryocytes

Myelodysplasia

200

myelodysplasia therapies

Bone Marrow Transplant is only curative

201

– van den Berghe Nature 1974
– severe anemia
– mild leukopenia
– normal or increased platelets
– atypical megakaryocytes
– indolent
– <5% blasts

5q treatment

5q syndrome

Lenalidomide

202

Myeloproliferative Disorders

• BCR/ABL(+): Chronic Myelocytic Leukemia
• BCR/ABL(-) & JAK2(+):
– Essential Thrombocythemia
– Myelofibrosis with Myeloid Metaplasia
– Polycythemia rubra vera
• JAK2(+/-): Chronic Myelomonocytic Leukemia

203

• 10% of all leukemias
• Adults>>>children
• Median age = 50
• M>F
• IR only known causative factor (Ionizing Radiation)
MPD - CML
• BCR/ABL
• “Philadelphia Chromosome”
Basophilia
– Fatigue / weight loss / night sweats
– Splenomegaly
– Leukostasis from Hyperleukosis
3 phases (Chronic, accelerated, blastic - acute leukemic transformation)

CML

204

CML treatment

Imatinib (Gleevec)

205

•Most common MPD
•Age at diagnosis: 50-60
JAK +
Bone Marrow = increased MEGS
•Near-normal life expectancy
– PLTS > 600K
– Microvascular Thrombi
– Bleeding
– Splenomegaly
– Recurrent first trimester abortions
– Leukemic transformation very low

Essential Thrombocytopenia

206

• 33% asymptomatic at diagnosis
• Fatigue / Weight loss / Fever / Night sweats
• Anemia
• Splenomegaly
– Leukoerythroblastosis
– Single or multiple cytopenias
• Bone marrow - fibrosis - “Dry tap” – Fibrous tissue takes place of normal BM tissue
• Leukemic transformation in 20% during first decade

MYELOFIBROSIS WITH MYELOID METAPLASIA

207

• Affects all 3 cell lines - RBCs the most
• Proliferate without EPO
• Serum EPO levels are low
• Median age = 60
• Increased HGB/HCT/RBC mass
• Bone marrow: Hypercellular
• B12 increased from increased WBCs producing B12-binding protein
• Symptoms related to increased viscosity
– Plethora
– Erythromelalgia
– Pruritus
• Arterial/Venous Thrombosis
• Thromboses:
» Renal/portal veins
» Budd-Chiari
» Mesentery

Polycthemia Rubra Vera

208

– Most common neoplasm in

ALL

209

ALL sites

Marrow usually

210

ALL presentation

– Bulky adenopathy
– Mediastinal mass
– Pleural effusions
– +/- hyperleukocytosis

211

ALL Lab

– ↑ WBC or Pancytopenia +/- Blasts
– LDH (= tumor burden)
– Hypercalcemia
– ↑ Uric acid / LFTs / BUN

212

ALL treatment phases

– Induction
– CNS
– Consolidation
– Maintenance

213

• Uncontrolled prolifeation of myeloid progenitors
• Replaced hematopoietic elements
• Ineffective hematopoiesis
• Majority de novo
• Treatment related
– Chemotherapy: CHR: -5 / -7 / 11
– RT
Auer Rods

– Bone marrow failure
– Abnormal hemostasis
• Thrombocytopenia
• Coagulopathy
• DIC most common with APL

214

• Lymphoid Neoplasm
• Binucleate giant Reed-Sternberg cell
• 75% of pts can be cured
• Origin
– Germinal B Center lineage
• Other adenopathies
– Mononucleosis
-EBV

Hodgkin's Lymphoma

215

Hodgkin's Lymphoma clinical features

– Adenopathy
• 80% Cervical
• 50% mediastinal
• Nontender / firm-pliable
– B symptoms
• Fever
• Night sweats
• Weight loss
– Other symptoms
• Fatigue
• Weakness
• Anorexia
• Etoh induced node pain
• Pruritus

216

review difference between B cells and T cells

• B cell
– Produced and mature in marrow
– B cell receptor
– Antibody production
– Plasma cells
• T cell
– Produced in marrow
– Mature in Thymus
– T cell receptor
– CD4: Helper T cells
– CD8: Cytotoxic T cells

217

t(2;5)
t(8;14)
t(14;18)
t(11;14)

ALCL
Burkitts
Follicular
Mantle

218

– Family History
– Previous neoplasm
– Immune suppression
– Infection
– “B” symptoms
– Weight loss: >10% weight in 6 months
– Fever
– Night sweats
• Physical examination
– All node bearing regions including Waldeyer’s
– Organomegaly
– Skin involvement

NonHodgkins Lymphoma

219

Non Hodgkins types

• INDOLENT
• Chronic Lymphocytic Leukemia
• Follicular Grade 1/2
• MALT
• Lymphoplasmacytic Lymphoma
• AGGRESSIVE
• Follicular Grade 3
• Diffuse Large Cell
• Anaplastic Lymphoma
• Mantle Cell Lymphoma
• Primary CNS Lymphoma
• Acute Lymphoblastic Lymphoma

220

• Median seventh decade
• BM-PB-LN/L/S
• SLL = tissue equivalent of CLL
• Incurable/median survival ~ 10 YRS
• Can transform to:
– Prolymphocytic leukemia
– Large B Cell lymphoma (Richter’s)
• Treatment
• Oral agents - Chlorambucil
• IV/Biologics - Rituximab

CLL

221

• Also called Waldenstrom’s macroglobulinemia
• median seventh decade
• BM/LN/S
• Rarely – PB / extranodal
• IgM elevated
Very high = hyperviscosity
• Generally incurable
• MS ~ 9 YRS

Lymphoplasmacytoid Lymphoma

222

• Median sixth decade
• 35% of NHL
• BM/LN/S/Extranodal
• May transform to aggressive
• Early stage - therapy
• Advanced stage not curable
– Initial treatment may be surveillance
t14:18

Follicular Grade 1 or 2

223

• Median seventh decade
• Three subtypes: MALT/Nodal/Splenic
• Can be nodal or extranodal
• Extranodal often with Autoimmune disease
• Sjogren’s
• Hashimoto’s
• H.pylori gastritis
• Incurable – MS ~ 10 YRS.
• Early MALT treat with antibiotics

Marginal Zone

224

• Median seventh decade
• M>>F
• t(11;14)
• Increased Cyclin D1
• BM/LN/Extranodal sites
• Lymphomatous polyposis
• Incurable
• Shorter MS – 3-5 YRS

Mantle Cell

225

• 30% of lymphomas
• Median age sixth decade
• Extranodal in 40%
• Curable with chemotherapy
– Most with early stage
– 50% with advanced
• CNS prophylaxis occasional

Diffuse Large B cell lymphoma

226

• Most common Pediatric NHL
• African = “Endemic” Form = EBV +
• Western
– Adults
– Sporadic
– EBV -– Mesenteric LN
– Ileum
– Cecum
– Liver - Spleen
• Curable with aggressive therapy
• CNS prophylaxis required
t8:14

Burkitts

227

– Cutaneous & systemic
– Systemic form
• children & adults
• Expresses t(2;5)
• Mainly T cell
– Cutaneous
• Mostly adults
• Isolated skin nodules
• Is more indolent and incurable

Anaplastic Large Cell

228

• Cutaneous T Cell lymphoma
• Multiple cutaneous plaques – nodules
• Generalized erythroderma
• Treatment often topical

Mycosis Fungoides

229

• In HTLV-1 areas:
– Japan
– Carribean
• Presentation:
– High WBC
– HSM
– Hypercalcemia
– Lytic bone lesions
• CD-30+ = Ki-1
• t(2;5)
• Four clinical presentations:
– Smoldering
– Chronic
– Lymphomatous
– Acute

Adult T cell Leukemia/Lymphoma

230

• Incidence 60x greater than general population
• Median age fourth decade
• Usually ST III/IV
• Often extranodal: GI/BM/CNS
• Primary CNS lymphoma common in this group
• 70% = large B Cell / other = Burkitt-like

Lymphoma HIV associated`

231

Typles of plasma cell neoplasms

• Clinically Benign:
– MGUS
• Indolent:
– Waldenstrom’s
– Indolent Myeloma
• Malignant: Plasma Cell Myeloma
• Malignant Aggressive: Plasma Cell Leukemia

232

• Definition:
– M Protein(G,A,M)Value < 3.0 g/dl
– No Urinary Light Chains
– Normal
• CBC
• Renal function
• Calcium
• Bone
– Bone marrow plasmacytosis < 10%

MGUS

233

1. Monoclonal protein serum a/o urine
2a. Plasmacytoma OR
2b. Marrow plasmacytosis > 10%
3. CRAB:
• Calcium
• Renal - light chain tub interst nephritis
• Anemia
• Bone - osteoporosis
Rouleax formation

Multiple Myeloma

234

Myleoma symptoms

back pain
headache
blurry vision
CHF
Sausage retinal veins

235

Collection of plasma cells usually in vertebral body

Solitary Plasmacytoma (treat with bisphosphonates)

236

virchows triad

– Venous stasis
– Blood vessel damage
– Hypercoagulability

237

Disorders of Thrombosis -Prophylaxis in Podiatric Surgery
3 significant risk factors

– Prior VTE
– Hormone replacement/Oral Contraception
– Obesity

238

– Most common heritable risk factor
– Factor V resists lysis by Prot C
– Caucasians: 5% incidence
• Majority = no thrombosis
– 20% with VTE +
– VTE risk increased by other risk factors

Activate Protein C Resistance

239

• Increase O2 carrying capacity
• Not for volume replacement
• Symptomatic anemia / acute hemorrhage
• Increase HGB in adult ~ 1 GM / DL

Packed RBCs

240

• Replaces volume and O2 carrying capacity
• <1% of all xfusions
• Large amount of plasma

Whole Blood

241

• Wash with saline to remove plasma
• Indication – repeated hypersensitivity reactions

Washed RBCs

242

• Remove WBCs by filtration
• Indication – multiple non-Hemolytic transfusion reactions

Leukoreduced RBCs

243

– From whole blood
– Preserves labile proteins except Factors V & VIII
– Efficacy limited by:
• Shortest ½ life of factor being replaced(Often Factor VII)
• Degree of factor deficiency
– ABO compatible
– Indications:
• Replace coagulation factors
• Factor deficiencies
– With bleeding
– Scheduled for surgery
• DIC
• Liver disease
• Rapid reversal of warfarin

Fresh Frozen Plasm

244

– Cold soluble proteins left when FFP is thawed.
• FVIII / FXIII / Fibrinogen
• vonWillebrand’s Factor
– Replacement of Fibrinogen
– ABO not needed
– Indications:
• Deficiencies:
– Fibrinogen
– F XIII
• DIC
• Hemophilia A or vWD (when no FVIII concentrate)

Cryoprecipitate

245

• Diagnosis of exclusion
• Common:
– 1% of RBC
– Up to 30 % of PLT xfusions
• inc temp. ≥ 1 deg F near end or following
• Recipient ATB vs. Donor leukocyte ATG
• Symptoms:
– Hallmark is fever
– Chills / Hypertension / Tachycardia
• Usually transient

Febrile Nonhemolytic Transfusion Reaction

246

– Most=ABO incompatible
• Often mislabeling or wrong ID
– 1:25,000
– Mortality 17-60%
– Fever/chills/dyspnea/chest pain
– Shock-death
– Hallmark = Intravascular hemolysis:
• Complement fixation by IgM
• Hemoglobinemia - Hemoglobinuria
– Direct Coomb’s = +
– Indirect Bili
– Jaundice
– ATN

Acute hemolytic transfusion reaction(immune

247

• Rapid extravascular clearance of xfused RBCs
– Immunized prior xfusion(“primary”)
– Days or weeks
• May be mild and unnoticed
• More common than acute: 1:7000
• Hallmark = unexplained decrease in Hgb
• Fever / chills
• Lab:
– Increase Bili / LDH / reticulocyte count
– Jaundice
– DAT usually +
– Decrease in Haptoglobin

Delayed Hemolytic Transfusion Reaction

248

• Small amount
• Sudden onset & rapid progression
– Respiratory distress
– Vascular collapse
– Afebrile
• IgE response to transfused proteins
• Particularly susceptible IgA deficients

Anaphylactic Reaction

249

• Noncardiogenic pulmonary edema
• Usually ~ 2 hours after xfusion
• Acute respiratory insufficiency & hypotension
• CXR = bilateral white out
• Fatality 7%

TRALI

250

Platelets are involved in _________ hemostasis

primary

251

How does thrombocytopenia present

– SPONTANEOUS BLEEDING
– PERSISTENT BLEEDING
– EASY BRUISABILITY(WITH OR WITHOUT TRAUMA)
– OOZING OF BLOOD - OFTEN FROM MUCOUS MEMBRANES
– UNEXPLAINED GI OR GU TRACT BLEEDING
– UNEXPLAINED RED FLAT PINPOINT RASH - OFTEN LOWER EXTREMITIES

252

- Intravascular purpura
- Platelet disorders
- <3mm
- Non-palpable

Petachia

253

thrombocytopenia bone marrow smear

increased cellularity
megakaryocytes

254

• Most common cause of easy bruising in a healthy adult
• Females > Males
• Decades 2 & 3
• Easy Bruising
• Diagnosis of exclusion
• Bone Marrow = Megakaryocytes OK
• No Splenomegaly
• Rx:Prednisone/Splenectomy/IVIG/Neumega/Romiplostim/Eltrombopag

Immune Thrombocytic Purpura

255

– dec Platelets and fibrinogen
– inc FDP - PT - PTT - Thrombin Time
– inc D-Dimer:
• degradation of stabilized fibrin
• confirms thrombin generation & FXIII cross-linking
Non-immune get Schistocytes
– thrombosis - smaller vessels
– bleeding = Factor Consumption & Plasminolysis
– treat etiology

DIC
Diffuse Intravascular Coagulopathy

256

• Large vWF multimers
– Lack protease
• Thrombi: CNS - Kidneys - Myocardium
• Peak = 20s F = 65%
• Clinical:
– Fever
– MAHA - Thrombocytopenia
– Neurologic - Renal
– Hematuria – Proteinuria
– Schistocytes - NRBCs
– Normal: PT/PTT/fibrinogen

TTP

257

• Children>Adults
• Prior Infection
• vWF protease normal
• MAHA / Thrombocytopenia (< TTP)
• ARF (renal > TTP)
• No Neurologic or Fever

HUS

258

Platelet Transfusion - Parameters

– 60,000

259

Definitions of Hemostasis

• Primary: Platelet Plug:
• Platelets + vascular injury = platelet plug
• Requires VWF + FVIII
• Activates secondary
• Secondary: Fibrin Plug:
• Activation of the coagulation cascade = fibrin plug

260

Disorders of Hemostasis - Coagulation Cascade

• Extrinsic (Checked with PT/INR)
– Tissue Factor + FVIIa
– Converts X -> Xa
– PT/INR
• Intrinsic
• Initial sequence
– Vascular injury
– Kallikrein activates F XII
– Cascade follows
• aPTT

261

– Prolongation: dec in Fs II/V/VII/X/Fibrinogen
– Extrinsic system abnormalities
– INR(Int. Normalized Ratio) for Warfarin patients

Prothrombin Time(PT

262

Prolongation is dec for factors II/V/VIII/IX/X/XI/XII
– Intrinsic system
– Rarely affected by fibrinogen

aPTT

263

Disorders of Hemostasis - Mixing Studies

– Prolonged PT / aPTT from deficiency?
– Mix patient and control plasma
– Correction
• qualitative or quantitave factor abnormal
– Noncorrection = factor inhibitor
• Lupus anticoagulant
(Mix w/normal control. If PTT is corrected it means there is a deficiency (Present with bleed,
bruise) If it doesn’t correct then SLE (these will present with thrombosis)

264

Abnormal PT

– Vitamin K deficiency
• Vitamin K dependent factors measured by PT = II/VII/X
– Coagulopathy of liver disease
• Initial = Decreased F II/VII/X
• Factor V
– NOT Vitamin K dependent.
– Hepatic disease vs. other prolonged PT

265

abnormal aPTT

– Hemophilia
• A = congenital def of F VIII
• B = congenital def of F IX
– von Willebrand’s disease
• dec vWBF = dec FVIII = inc aPTT
• Corrects on mixing
– F XII Deficiency
– LA
• no correction with mixing

266

Abnormal PT + aPTT

– Coagulopathy of liver disease
– Deficiencies of individual factors
• Factor II (Prothrombin)
• Factor X (Stuart-Prower)
• Factor V (Proaccelerin)
– DIC
– LA

267

cuases of ataxic gait

posterior column disease
cerebellar degeneration
peripheral neruopathy

268

Steppage gait causs

LMN disease such as neuropathies (syphillis) Tabes dorsalis

269

Stiff spinal cord gait - circumduction gait

UMN disease

270

Magnetic gait

Normal Pressure Hydrocephalus

271

glasgow coma scale

Eye
Spon 4
resp to speech 3
resp ot pain 2
No respons 1

Motor
Obeys 6
Localizes 5
Withdraw 4
abn flxr 3
abn ext 2
no response 1

verbal
oriented 5
confused 4
inappropriate 3
incomprehensible 2
no response 1

15 = wnl, < 8 fatal, 3 = dead

272

Resting tremor
unilateral
cogwheel rigidity
Bradykinesia
asymmetric onset
treatment

Parkinsons disease

start with levodop or dop agonist first to control symptoms

273

Less tremor than parkinsons
vertical gaze impaired
Stiff gait --Fall backward
Axial rigidity, hyperextended
Falling is big concern

Progressive supranuclear palsy

274

An action tremor with a high amplitude and high-frequency.
Tremor kicks in when you use your hands for example
Bilateral, postural and action tremor
Duration > 3 years
Family history
Alcohol response – worse with alcohol
Otherwise neurologically normal

Essential tremor

treatment
mysoline and BB

275

Usually occurs in young people (mean is 29 years)
Optic neuritis (Loss of vision, double vision, Internuclear Opthalmopelgia)
Vertigo/Diszziness & Insomnia, Oropharyngeal problems – dysphagia, slurred speech
Demyelinating lesions are found in the brain and spinal cord
Deep white matter plaques

Test to order

Multiple Sclerosis

cranial MRI with Gadolinium

276

Types of MS

Relapsing – Remitting (RRMS)
Seconary progression (SPMS)
RRMS with multiple increasingly frequent relapses
Primary Progressive MS (PPMS)
Clinically Isolated Syndromes suggesting MS (CIS)
Isolated single episode
Benign MS
15% don’t relapse
15% may have plaques at autopsy with no history of MS

277

acute flares of MS treated with

IV glucocortricoids

278

ACh Receptor Antibodies
10 to 15% of MG patients have thymoma (benign)
Fatiguibility that IMPROVES with rest
Ptosis – usually bilateral, but may be unilateral
Diplopia
Fluctuating weakness
Testing includes: Tensilon tests, EMG/NCV, Chest CT, ACh Receptor antibodies
Repetitive stimulation -> NCV decrement – due to ACh depletion

Myasthenia Gravis

Mestinon, Immunosuppressant
Avoid NM blocking drugs

279

Antibodies against voltage gated calcium channels – impairs Ach release
Almost all are > 40 y/o
Most are paraneoplastic in nature
Think Cancer! -> Small cell of lung, Lymphoproliferative disorder, pancreatic cancer, ovarian
cancer, Breast cancer
LEMS precede cancer by 1 year
Looks just like MG
Proximal weakness (LE > UE)
Easy fatigubility
Strength and DTRs may improve after isotonic exercise
Dysautonomia more common than MG -> especially dry mouth!
EMG/NCV
Increment on NCV after repeat stimulation (not decrement)
Treat by finding cancer and treating that

Lambert Eaton Myasthenic Syndrome

280

UMN and LMN disease; CNS & PNS
Loss of Motor neurons in corticospinal tract
Eventually may get frontal lobe dementia
Hyperreflexia, Atrophy, Fasciculation, Weakness, Spastic, Painless usually
Skeletal muscles -> eventually diaphragm
EOM only muscles spared
Pure motor disease
Above levels also affected
Dx via EMG!! – not NCV
Supportive Care; Riluzole may prolong life expectancy by 3 months

ALS

281

Can be Compressive myelopathy
Motor and sensory symptoms
Below level affected

Spinal stenosis

282

Meylopathy
"Cape-like numbness",
Symptoms of myelopathy include paraparesis and a sensory level
Intraxial widening of the central canal

Syringomyelia

283

Pathology of the spinal cord

myelopathy

284

myelopathy signs and symptoms

Spasticity
Upper motor neuron
Sensory level
Bladder and bowel incontinence
Pain
Characteristic gait: Stiff and erect (Stiff Man Gait)

285

A febrile diabetic with back pain and myelopathy has what?

epidural abscess til proven otherwise

286

Acute; (+) Straight leg test
Front of leg = L3/L4; Lateral = L5; Radiates to heel = S1
Sensory & reflex changes usually immediate w/ onset of pain

sciatica

287

Confused w/ cellulitis & DVT
Usually post-op
 Severe hypersensitivity w/ swelling & sweating

CRPS/RSD/Causalgia

288

Desire to move legs
Feeling of motor restlessness
Worse with rest or at night
Better with activity
dx by history

Restless leg syndrome

289

Drugs taht cause tremor

beta agonists (sympathomimetics)
Lithium
Antipsychotic
Valproic Acid

290

Drugs associated with PerNeur

amidoraone
vincristine
metrnidazole
halothane

Vincristine
B-6
INH are the biggies

291

drugs with myopathis

statins
steroids
accutane
chloroquine

292

General myopathy symptoms

Painful Myalgias
Cramps
Contractures
Myotonia - Stiff
Myoglobinuria
No weakness, fatigue, exercise intolerance, muscle atrophy

293

Boys
Absent dystrophin
Pseudohypertrophy
Positive Gowers sign
Cognitive imparitment
Waddling gait
Cardiac probs
High CPK

Duchenne's

294

myopathies vs NMJ

NMJ Diseases generally involves proximal muscular weakness and is symmetrical.
See MG and LEMS above

295

Endocarditis or arrhythmia associate with what stroke

embolic

296

HTN with what stroke

Lacunar

297

CAD with what stroke

thrombotic

298

Collective term that refers to different types of motor behaviors that are present in patients who
have lesions of the descending corticospinal system

Spasticity

always think brain or spinal cord

299

common causes of spasticity

Stroke
Cerebral Palsy
Traumatic brain injury
Anoxia
Spinal cord injury
MS
ALS, PLS, MSA
Metabolic diseases (Leukodystrophies)

300

treatments for spasticity

Benzodiazepines,
Baclofen,
Tizanadine (Zanaflex)
Botox.
Also PT, serial casting, orthoses, orthopedic procedures

301

Unilateral
pulsating
moderate to severe
aggrevated by activity
Photo & or phonophobia
prodrome -> aura -> HA -> post drome

migraine

302

types of migraine

common - no aura
classic - aura
complex - focal neuro deficity
basilar - HA, N, vertigo

303

tx for migraine

non pharm - foods, etoh, caff

acute - nsaids, ergot, steroids, narcotics

preventative - TCA, CCB (2nd) BB, Depakote, botox

304

Unilateral
severe ice pick
retroorbital
stiffness, rhinorrhea,
occur in clusters
smoker

cluster

02, steroids, lithium CCB

305

base of skull to temporal region
band like
palpable muscle tension
stress
overlap with migrain
30 min to 7 days
pressing or tightening

tension

306

worst HA of my life

sub-arachnoid hemorrhage

neuro emergency

307

parkinsonisms
frontal visuospatial dementia
fluctuating cognition
recurrent visual hallucination
lang and mem still good

Lewy body dementia

308

magnentic gait
incontinenc

normal p hydrocephalus

309

How are peripheral neuropathies classified?

Acute
Chronic
Motor
Sensory
Compression
Hereditary
Axonal – Lower Amplitude
Demyelinating – Slower amplitude

310

myelinopathies types

acute - guillian barre
chronic

311

Antibodies cross react with antigens on Schwann cells
Associated with infections above
Progression over course of 2 to 4 weeks with nadir by 2 weeks
If longer than 8 weeks think CIDP
Ascending symmetric weakness*
DTRs absent*
Tingling dysesthesia
EMG/NCV shoe conduction block or prolonged motor velocities
CSF shows elevated protein and pleocytosis of 10 lymphocytes
Treatment is Plasma exchange or IVIG within 7 days of onset

guillan barrre

312

NM disease
DTR intact
Perioral numbness
dysphagia

botulism

313

rule of 9's for glial based tumors

grade 4 - GBM - 9 mo to live
grade 3 - astrocytoma - 18 mo to live
grade 2 - glioma - 27+ mon

314

Signs and symptoms of osteoporotic fracture

height loss, kyphosis, or unexplained back pain
previous or current facture

315

mechanism of bisphonsphonates

*1. Inhibition of osteoclast formation
*2. Inhibition of osteoclast activation
*3. Inhibitation of mature osteoclast activity
*4 Reduction in osteoclast life span-apoptosis
Can cause Jaw osteonecrosis & frozen bone

316

PTH analog

Teriparatide

317

Actions of cortisol

• Primary active glucocorticoid
• Antagonizes insulin secretion and action
• Stimulates gluconeogenesis
• Impairs protein synthesis in bone, skin, muscle and connective tissue
• Impairs macrophage production of inflammatory cytokines
• < 5% cortisol is free, physiologically active, and still filterable by the kidney
• Circadian cycle
– Peak before waking; nadir before sleeping

318

Actions of aldosterone

• Primary mineralocorticoid
• Stimulates Na+ / K+ sodium pump in the renal collecting duct
– Minor Na+ retaining actions also on salivary ducts, sweat glands and GI tract

319

actions of androgens

• DHEA and androstenedione are produced mainly in the Z. reticularis
– Weak androgens, but converted to testosterone (a more potent androgen) in the testes
• In males, adrenal androgens of little significance
• In females, adrenal androgens are the major source of androgens and responsible for the
development of pubic and axillary hair and for libido

320

Stimulation testing

• For adrenal cortical insufficiency

• ACTH (cosyntropin) stimulation test
– IV ACTH stimulates an appropriate cortisol response in normals

• Furosemide stimulation test
– IV furosemide then 3 hours upright stimulates an appropriate aldosterone response in normals

• Metyrapone stimulation test ( for secondary adrenal cortical insufficiency)
– Oral metyrapone impairs cortisol production resulting in an appropriate ACTH rise in normals

321

Suppression Testing

• For adrenal cortical hyperfunction

• Dexamethasone suppression test
– 1 mg of dexamethasone orally at midnight lowers 8 AM plasma cortisol level in normals

• Saline suppression testing
– Normal saline at 500 cc/hr for 4 hours lowers serum aldosterone level in normals

322

– Muscle weakness; fatigue; weight gain; possible diabetic symptoms; menstrual changes;
emotional changes; skin changes
• Signs
– Cushingoid facies; centripetal obesity; “buffalo hump”; edema; abdominal stria; hirsutism;
HBP; osteoporosis

Cushing's Syndrome

Iatrogenic most common

323

Cushing’s Diagnosis

– Elevated plasma cortisol
– Dexamethasone suppression test failure
– ACTH may be elevated or low

324

Cushing’s Treatment

– Pituitary or adrenal surgery
• Adrenalectomy with replacement therapy conveys a 10% risk of a pituitary tumor w/in 10 years
– Steroidogenesis inhibitors (e.g., ketoconazole, mitotane)
• Generally reserved for poor surgical candidates

325

adrenal adenomas are common
t/f

true

326

• Usually 2° to an adrenal adenoma
– possibly 2° to cortical nodular hyperplasia
• Generally presents as hypertension with hypokalemia
– Possibly accounts for up to 5% of hypertensive patients
– Usually no edema 2° to “escape phenomenon”
• Diagnosis
– Elevated aldosterone levels
• Plasma aldosterone concentration (PAC) and plasma renin (PRC) concentration:
– PAC / PRC > 30 highly suggestive
– Failure to suppress aldosterone with normal saline suppression testing

Primary aldosteronism (Conns syndrome)

327

Secondary aldosteronism

• Usually renovascular disease (e.g., renal artery stenosis)
– Rare renin producing tumors (e.g. juxtaglomerular cell tumor)
• Edematous conditions (e.g., cirrhosis; nephrotic syndrome; CHF)
– “third space” fluid but arterial hypovolemia prompts aldosterone release

328

• Symptoms and signs
– Fatigue; weight loss; nausea and vomiting; “bronze hyperpigmentation”; hypotension
• Diagnosis
– Low serum cortisol; elevated ACTH
– Hyponatremia with hyperkalemia
– Inadequate cortisol response to ACTH stimulation test

Primary adrenocortical insufficiency
(Addison's Disease)

329

treatment for addisons

– Hydrocortisone 20-30 mg daily
– Fludrocortisone 0.05-0.1-mg daily

330

• Possible panhypopituitarism
• Generally iatrogenic
– Rapid withdrawal from long-term steroid therapy
• Especially fluorinated steroids
– Medications (e.g., Dilantin, ketoconazole, rifampin, mitotane)
• Alternate day prednisone to preserve HPA axis
– e.g., prednisone 20 mg every other day; tapering from 10 mg of prednisone daily to 10
mg and 5 mg on alternate days, then 10 mg every other day, etc.

2ry adrenocortical insufficiency

331

• Hypovolemic cardiovascular collapse
– Fatal if unrecognized

addisonian crisis

332

addisonian crisis tx and prevention

• Treatment
– IV Hydrocortisone 100-mg bolus followed by 10 mg / hour continuous infusion
• Prophylactic stress steroids
– 75-100 mg of hydrocortisone daily
– Hydrocortisone 100 mg IV preoperatively

333

– Symptoms
• Paroxysmal beta adrenergic symptoms
– Laboratory findings
• Urinary free catecholamines, VMA, metanephrines
– CT scan tumor localization

Pheochromocytoma

334

treatment for pheochromocytoma

phenoxybenzamine

335

type 1 DM clinical manifestations

polydipsia
polyuria
polyphagia
Ketosis-prone
absolute insulin deficiency

336

infants and children first manifestation of Type 1 DM

ketoacidosis

337

type 2 clinical manifestation of type 2

recurrent infections
genital pruritis
hyperglycemia,
visual changes
parasthesias and fatigue

338

effects of hyperglycemia

glycation of proteins (hemoglobin, collagen)
accumulation of sorbitol and fructose (nerves, lens)
activation of protein kinase C (vascular cells)

339

Diagnositc criteria for DM

 Hemoglobin A1c 6.5,
 FBS 126,
 2 hour postprandial glucose 200
 Diagnostic criteria for IFG (FBS 100-125);
 Diagnostic criteria for IGT (2-hour postprandial glucose 140-199);
 Hemoglobin A1c 6.0-6.5 "high risk" for diabetes

340

type 1 general treatment

insulin
lifestyle modification
--no glycemic control

341

General treatment of type 2

diet, exercise, drugs
Glycemic control

342

 Mechanism of action: Decrease hepatic glucose production
 Little risk of hypoglycemia;
 Lactic acidosis with CHF and renal failure;
 Weight neutral
Insulin secretagogues:

metformin

343

insulin secretagogues names

sulfonylureas (glyburide, glipizide)
repaglinide
nateglinide

344

 Mechanism of action: Increase basal and/or postprandial insulin secretion
 Hypoglycemia can happen
 Weight gain can happen

Sulfonylureas/glyburide:

345

Possibly useful before the heaviest meal of the day

Meglitinides/nateglinide

346

 Suppresses appetite;
 Weight loss;
 Improved insulin sensitivity;
 Injectable

GLP-1 agonists/Exanatide:

347

 Oral; similar to GLP-1 agonists but weight neutral

DPP-4 inhibitors/sitagliptin:

348

 Mechanism of action: Enhance tissue response to insulin
 Weight gain
 CHF risk
 long bone fracture risk

TZDs/pioglitazone:

349

generally start type 2 DM meds with what

metformin and/or a sulfonylurea

350

insulins - short, normal and long acting

aspart, glulisine, lispro - 4-6 hrs
regular - 6-8 hrs
NPH 12 -20 hrs
Ultraiente 18-24 hrs
Glargine 24 hrs

351

70/30 dosing

most common insulin regimen
70% NPH and 30% regular

morning dose covers glucose values before dinner
evening covers fasting glusoce

352

explain 70/30 dose adjustment

the patient takes 20 unitls of 70/30 before breakfast and supper but has hypoglycemic symptoms before supper but a consistent fasting

Adjust 70/30 to 15 before breakfast and 25 before supper

353

basal bolus isulin

basal one dose
bolus based on carbs 1:15 CHO
--short acting

354

other DM goals

 Diabetic LDL <125/70 if nephropathy

355

polydipsia, polyuria, polyphagia, fatigue, dyspnea, nausea / vomiting,
abdominal pain, dehydration and may have been precipitated by an acute illness,
fruity breath, tachycardia, tachypnea
met acidosis
hyperglycemia

Diabetic ketoacidosis

356

tretment for DKA

IV fluid replacement
--noarmal saline at 1000 cc/hr
--expect rapid K+ decline with insulin and add 20-30 mEQ KCl/hour if K+ < 5.3
----hold insulin therapy if admision K+ is < 3.3
Regular insulin
NaHCO3 - only if pH < 6.9

357

DKA stymptoms but without met acidosis

and diff in treatment

Hyperglycemic Hyperosmolar State

Never give bicarb

358

most common cause of hypothyroidism

iodine worldwide
hashimotos in developed countries

359

t4 low
tsh normal

2ry hypothyroidism

360

tired
dry skin
cold
poor memory
constipagtion
weight gain
t4 low
tsh high

hypothryoidism

361

floppy baby
umbilical hernia
large tongue
neuro damage
pericardial effucsion

cretinism

362

hypothyroid tx

t4 replacement
levothyroxine at 50mcg
wait 3 to 6 weeks to equilibriate

363

AI dissorder
HLA DR4
may have FH of AI dsease
females
TSI
TSH low
t4 high
hyperactive
heat intolerant
palpitations
fatigue
wt loss
thryomegaly
tachycardia
exopthalmose

hyperthyroidism

364

graves treatment

beta blockers (propranolol)
sometimes tpo inh
--propylthriuracil, methimazole

365

average age 60
goiter
thyroid lymph infiltrate
elevated TSH, low t4,
TPO and anti-TG antibodies
enlarged cystic nodular thyroid
hypothyroid symptoms

hashimotos

366

Acute onset
mimic pharyngits/URI
Thyroid tender to palpation
hyperthyroid 1 mo - then hypoth 1 mo
initially elevated ESR

tx

Viral thyroidits

Treat with nsaids

367

What compounds and medications interfere with a thyroid uptake and scan

Imaging Studies
– Radioactive iodine uptake reflecting thyroid activity; also helpful for thyroid nodules
– Beware of iodine-containing contrast media, thyroid medications, etc. for about 6 weeks
prior to the scan**
– “Hot” (autonomously functioning) nodules are nearly always benign
– “Cold” nodules are usually benign, but are more likely malignant than “hot” nodules

368

“stones, bones and groans”
sually caused by adenoma
hypercalcemia
hypophospatemia
high PTH
osteoporosis
osteomalcia
kidney stones
muscle waekness

hyperparathyroidism

369

 “classic” subperiosteal bone resorption with prolonged disease, often involvin phalangeal tufts
– rarely seen in developed countries anymore

 Osteitis fibrosa cystica
primary hyperparathyroidism

370

gold standard for primary hyperparathyroid

surgical treatment

can use calcitrol
vit D
cinacalcet

371

 Hypocalcemia
 Hyperphosphatemia
 Tetany; increased nerve excitability; uncontrolled cramp-like spasms of hand, feet, arms, face
Usually Iatrogenic
 Convulsions
 Trousseau’s Sign positive

tx

primary hypoparathyroidism

calclium and vit D

372

 Excessive calcium intake along with absorbable alkali (e.g. baking soda) overwhelms kidneys ability to excrete excessive calcium
 Hypercalcemia, metabolic alkalosis and renal insufficiency

Milk Alkali syndrome

373

Hypercalcemia Treatment

 Normal saline
 Sodium increases calcium excretion; treats (the usually underlying) dehydration
 Furosemide
 Impairs calcium reabsorption
 Bisphosphonates
 Impair bone resorption
 Calcitonin
 Impairs renal calcium reabsorption and bone resorption
 Corticosteroids
 Increase renal calcium excretion and impair calcium absorption from the gut

374

 Myalgias, muscular weakness, cramps and fasciculations; ultimately tetany
 Irritability and paresthesias; ultimately seizures and increased intracranial pressure
 Signs
 Chvosteck and Trousseau signs
May be caused by mg def, vit d def

Hypocalcemia

375

Most common cause – H. Pylori
Duodenal (90%) and gastric ulcers (70%)
PUD
NSAIDs – 2nd

tx

ulcers

antisecretory therapy plus antibiotics

376

Reflux disease treatment

Antacids (Tums)
-intermittent mild symptoms
H2 blockers (ranitidine, cimetidine, famotidines)
-Mild to moderate, more consistent symptoms
-Heals erosive esophagitis in 8 weeks
Sucralafate (Carafate)
-Bile Reflux
Proton Pump inhibitors (Omeprazole, lansoprazole, -prazoles)
-All levels of symptoms severity
-Heals erosive esophagitis in 4 weeks in 70% of patients
-Heals erosive esophagitis in 8 weeks in 90% of patients

377

Difficulty swallowing
Most often due to esophagitis, peptic benign stricture
Less often cancer of the esophagus or a motility disorder like achalasia
usually caused by reflux

dysphagia

378

Painful swallowing
Most often due to infectious esophagitis
Viral like herpes or CMV
Fungal like Candida esophagitis
Pill induced esophagitis
tetracycline, potassium; quinidine and bisphosphonates

Odynophagia

379

what do you do first for dyshpagia

If you suspect the dysphagia is due to an esophageal origin should undergo an upper endoscopy
If unsure if it is esophageal or pharyngeal do an upper endoscopy to rule out an esophageal cause
You don’t want to miss an esophageal malignancy

380

But not in place of endoscopy
Will show Stricture, Mass in esophageal cancer and in peptic stricturs

barium swallow

381

Classic dilated esophagus
Bird’s beak appearance
Due to tight LES
Best seen on Barium Swallow

achalasia

382

History of Reflux or Barrett’s esophagus
Now has Solid food dysphagia
Weight loss

adenocarcinoma

383

History of Reflux
Now has Solid food dysphagia
NO weight loss

peptic stricture

384

History of intermittent dysphagia
Solids, especially breads and meats
No weight loss

Schatzki’s Ring or a Cervical Web

385

scc of esoph

tobacco and alcohol
women
proximal to mid esop

386

adenocarcinoma of esoph

barretts
white males
distal esoph/gastric cardia

387

History of intermittent dysphagia
Liquids or Solids & Liquids
No weight loss

achalasia

388

If patient has rectal Bleed first check

if orthostatic
may need to give fluids or resescetate

389

Intermittent Diarrhea without blood
Especially young woman
May be associated with bloating and abdominal cramps
No weight loss
Rarely nocturnal diarrhea

IBD

390

Middle age or eldery
Blood mixed with stool
Several months
Now has lightheadedness
Iron Def anemia

how to diagnose

Colon cancer

colonoscopy

391

Elderly
History of Coronary Heart disease
Few episodes of bloody bowel movement for 1 to 2 days
Occurred with abdominal pain
Hgb typically drops only 1 or 2 grams

Ischemic colitis

392

Any age
Very Short duration of bloody diarrhea
Associated with ab pain and fever

infectious diarrhea

393

Elderly
Mult episodes of painless! large bloody bowel movements
Primarily made up of blood
May be orthostatic
Labs show decreased hgb and hct
Hgb may drob several grams from baseline
If no evidence of upper GI bleed
Most common cause of hemodynamically significant lower GI bleed in elderly
Aorto-enteric fistula

diverticular bleeding

394

Massive bleeding from rectum
History of repaired abdominal aortic aneurysm
Very unstable due to large amount of bleeding

Aorto-enteric fistula

395

Microscopic
Found only by positive hemoccult test
Clinically significant
If Cecal AVM – Red blood or melena
If Small Bowel AVM – Melena

Bleeding from Arteriovenous Malformations

396

Hematemesis
Ab pain
History of being on NSAIDs
May have coffee grounds as well

PUD

397

History of recurrent non-bloody vomiting followed by bloody vomiting

Mallory Weiss tear

398

Coffee Ground emesis
History of heartbur

esophagitis

399

Significant LLQ ab pain
Fever
No rectal bleeding
Middle aged or elderly
No diarrhea usually
Diagnosed by CT scan
NO colonoscopy or barium enema
Can cause perforation

diverticulitis

400

Infection with C difficile
Multiple watery bowel movements
With or without blood
Ab pain and fever
Febrile with ab tenderness
Nursing patients on oncology floor, following chemo
OR any patient following a course of broad-spectrum antibiotics
Treat with metronidazole or vancomycin

Pseudomembranous colitis

401

Small bowel, especially terminal ileum
Transmural inflammation
Not usually continuous involvement of the bowel
Skip arease – areas of affected bowel interspersed with normal bowel
ASCA
Cobblestone
Colon not usually involved
Though it can be
Diarrhea but no blood
Pain more of a problem for them
Diagnosed with colonoscopy
Biopsies of terminal ileum, small bowel follow through, and capsule endoscopy
Treated with immunosuppressants and immune modulator therapy

Crohns

402

Only affects the colon
No small bowel
p-ANCA
Crypt abscess
Superficial ulceration of mucosal lining of colon
No skip areas – continuous
Rectum always involved
Multiple bowel movements every day
Small, frequent, soft, water, and can have blood
Diagnosed by colonoscopy with biopsies
Treated with anti-inflammatory agents and immunosuppression & (at times) immune modulator

Ulcerative colitis

403

Ulcerative colitis and Crohns
Extra-intestinal manifestations

Erythema nodosum
Pyoderma gangrenosum
Arthritis,
Iritis
Episcleritis

404

Small bowel disease
Presents with diarrhea
Large volume
No blood
Precipitated by ingestion of gluten
Protein losing eteropathy due to gluten
Actually sensitivity to gluten
Diagnosed by blood test for tissue transglutimase antibody
AND biopsy of small bowel during an endoscopic exam
Biopsy will show flattening of villi
AND accumulation of lymphocytes in lamina propria and epithelium
Treatment: Avoid food with gluten

celiac sprue

405

Used to detect a bleeding site when endoscopy or colonoscopy can’t find
OR when patient is bleeding too rapidly to safely do endoscopy
Often done prior to angiogram
Radio-isotope injected IV into patient
Images obtained at different time intervals to determine if a bleeding site can be found
To be positive, patient should be bleeding 0.5 cc’s per minute

Tagged RBC scan or Bleeding scan

406

Used to find and treat a bleeding site
Catheter into femoral artery
Dye injected into superior mesenteric, inferior mesenteric and celiac axis, & vessels they supply
If bleeding site found, can use a special coil or glue to embolize the artery (stop the bleeding)
To be positive, patient should be bleeding 1.0 cc per minute

angiogram

407

History of excessive alcohol use
Presents very ill
Jaundice and even febrile
AST > ALT; neither > 200
Bilirubin > 10, or even 20
High white count, like they have an infection (even though they don’t

alcoholic hepatitis

408

History of IV drug use, mult sex partners w/ prostitutes, or dirty needle for tattoo (neighbor)
Relatively ill on presentation
Viral syndrome – achy all over, febrile
Jaundice
RUQ tenderness
ALT > AST; both in high hundreds or thousands

Hep B acute

409

Presents same as Hep B
History of eating in questionable place
Or in contact with someone with disease
Or workers in Day Care

Hep A

410

Chronic disease
Usually asymptomatic, don’t know they have disease
History of blood transfusions, IV drugs, tattoo many years ago
ALT > AST but only mildly elevated; 100 to 250
Bilirubin normal

Hep C

411

History of attempted suicide or history of injury
Took more than recommended dose
If alcoholic, less need to have toxic effect
ALT > AST; usually very high, like in thousands
High bilirubin

Acetaminophen Hepatitis

412

History of significant hypotensive event
Heart attack or sepsis
Asymptomatic relative to liver disease
ALT > AST; usually very high, like in thousands
Bilirubin normal or slightly elevated

Ischemic hepatitis

413

You want to do an elective procedure on a patient with cirrhosis
t/f

false

414

hep b vaccinated vs immunity

vaccinated are positive for anti-HBs but not anti-HBc
Immune are positive for both

415

pharm and elderly

elderly have decrease in hepatic and renal metabolism so may need to decrease those drugs

416

bladder innervation

• Parasympathetic (cholinergic)
– S2-4: bladder contraction
• Sympathetic (alpha adrenergic)
– T11-L2: Bladder relaxation; bladder neck and urethral contraction
• Somatic
– Pudendal nerve: Pelvic floor muscular contraction

417

• Females
– Poor anatomic support / urethral dysfunction
• e.g., Multiparous female with pelvic floor relaxation (groceries, sneeze, pee)
• Males
– Sphincter damage
• e.g., Urethral sphincter damage from prostate surgery or radiation therapy

stress incontinence

418

• Local GU conditions
– e.g., tumor, stone, early obstruction, chr infection, adjacent GI inflamm or diverticulitis
• CNS disorders
– e.g., stroke, dementia, parkinsonism, SC lesions with impaired sympathetic innervation
• Idiopathic
– e.g., detrusor instability without GU or CNS disorder
Spastic bladder and UTI is usual cause

Urge

419

Dribblers
• Anatomic obstruction
– e.g., prostate hypertrophy, urethral stricture, large cystocele
• Poor bladder contractility
– e.g., diabetes, levels spinal cord injury with impaired parasympathetic innervation
• Neurogenic
– e.g., detrusor-sphincter dyssynergy

Overflow

420

 Chronic impairments of
o Cognitive function
o Mobility, Dexterity
 Environmental factors
 Psychological Factors

Functional incontinence

421

Post void residual volume

• BladderScan PVR
– Normal is < 200 cc
• Very helpful in distinguishing between overflow incontinence and either urge or stress
Normal UA but PVR is 300 -> Think overflow like a BPH

422

Treatment for Stress inco

behavior therapis
alpha adrenergic
estrogen
surgery*

423

treatment for urge

behavioral therapies
bladder relaxent drugs

424

treatment for overflow

surgery
catheterization*

425

 Nearsightedness
 Difficulty seeing objects in the distance

myopia

426

 Farsightedness
 Difficulty seeing near objects

hyperopia

427

 Impaired accommodation (ability to focus on close objects)
 Greek: “older vision”
 Universal; begins at about age 40
 Due to gradual age-related lens hardening & dimin muscular effectiveness of the ciliary body
 “PERRL”

treatment

presbyopia

reading glasses or bifocals

428

 Blurry vision (“dirty glasses”)
 Glare / “prism effect”, making it especially difficult to drive at night
 Age-related opacities tend to migrate centrally until they interfere with vision
 Predisposing factors
 Increasing age
 Diabetes
 Smoking
 Alcohol abuse

tx

cataracts

 Phacoemulsion with intraocular lens implants
 YAG laser capsulotomy in about 15% for subsequent capsular opacifications

429

 Most common cause of blindness in the elderly
 Characteristically central blindness
 Usually excellent peripheral vision

macular degeneration

430

 Drusen (yellow byproducts of metabolism) accumulate under the macula

dry macular degeneration

431

 Increasing drusen accumulation with angiogenesis and choroidal neovascularization

wet macular deg

432

treatment for macular deg

 Ocular vitamins (beta carotene 25,000 units, vit E 400 units, vit C 500 mg and zinc 80 mg)
 Laser phototherapy for neovascularization
 Intra-vitreal vascular endothelial growth factor inhibitor injections
 Stem cell research

433

 Characterized by ischemia, neovascularization, microaneurysms and hemorrhage.
 Importance of annual ophthalmologic examinations for diabetics
 Glycemic and antihypertensive control are both important

diabetic retinopathy

434

 Optic nerve head damage and visual field loss even with normal intraocular pressures
 Usually normal central vision with deteriorating peripheral vision
 “Tunnel vision”; “blinders”
 Aqueous drainage impairment leads to increased intraocular pressures

glaucoma

435

 aqueous drainage / filtration is slowed
 Usually asymptomatic and found on a screening exam by an eye professional
 Peripheral visual loss is slow and subtle

open angle glaucoma

436

 Aqueous drainage is blocked
 Usually acute and symptomatic
 Eye pain; headache; noticeable visual deterioration; possibly nausea and vomiting overshadowing eye pain
 Conjunctival injection
 May be provoked
 Mydriatics; darkness; lens enlargement from growing cataracts; infection; inflammation; trauma, etc

closed angle glaucoma

Give emergent treatment

acetolzaolmide while in ER

437

Glaucoma Treatment

 Eyedrops to suppress aqueous production
(e.g.,beta blockers; alpha agonists)
 Beware of systemic beta-blocker effects from eyedrops
 Eyedrops to facilitate aqueous outflow
(e.g., epinephrine, miotics such as pilocarpine, prostaglandins)
 Emergency iridectomy for closed angle glaucoma

438

• Common
• Thinning skin in an older persons external auditory canal produces thicker, drier and more adherent cerumen

Cerumenosis

439

 Generally results from past noise exposure, ototoxic drugs, cochlear neural atrophy or damage (e.g., encephalitis)
 Presbycusis (Greek: “older hearing”)
• Generally relatively symmetrical and bilateral
• High-frequency hearing loss predominates
 Phonemic regression
• Permanent hearing loss at the CNS level due to lack of stimulation (i.e., the brain “forgets” a frequency, and amplification is no longer helpful)

treatment

Sensorineural Hearing Loss

programmable digital amplification

not hearing aids

440

review rinne / weber

conductive - bone > air (cba)
----localizes to affected ear

ssn - air > bone
-----localizes to unaffected ear

441

the pathobiology of alzhiemeirs is characterized by

amylid plaques
neurofibrillary tangles

442

summary of dementia/depr/delirium

• Dementia
– Progressive cognitive decline; often, the patient “forgets that he forgets”
• Depression
– “vegetative” symptoms such as lack of motivation (“anhedonia”), sleep disturbances, appetite
and weight changes; flat affect
• Delirium
– Acute onset; delusions and hallucinations

443

A healthy 70-year-old man drank a little more
than usual with his friends at the American
Legion. He fell, fracturing his hip, which was
successfully pinned 3 days ago. His nurse calls
you at 10:00 PM because he is agitated, and he
claims that the CIA has bugged his hospital
room. He most likely has:

delirum

444

An 80-year-old woman complains of memory
problems and lightheadedness with exertion
during the past year, but she is otherwise
healthy, and she takes no medications except
for eyedrops for glaucoma. She most likely has:

• C. Beta-blocker-induced dementia

445

• A depressed 80-year-old widow complains that
her memory has worsened over the past 6
months. She has also noted generalized
muscular weakness, a worsening exercise
tolerance, visual disturbances, pedal edema,
cold intolerance and easy bruisability during the
past 6 months. She most likely has:

hypothroidism

446

A 76 year-old man’s wife complains that his
memory has never been the same since his
previous doctor gave him “rat poison” for several
“spells” of confusion and incoordination. He has
an irregularly irregular heart rhythm. The most
likely diagnosis is:

• D. Multi-infarct dementia

447

Test Question #2
• A 70 year-old man’s wife complains of his
increasingly worsening memory over the past 1 -
2 years. He is becoming more irritable, and he
gets lost occasionally when driving his car. He
most likely has:

alzheimers

448

A 75 year-old widow who gives a detailed
account of her poor memory ever since
the death of her husband 6 months ago
most likely has:

• C. Pseudodementia / depression

449

spastic hemiparises gait cause

CVA

450

Scissors gait cause

lower extremity spastic paresis from cervical spondylosis

451

assistive devices and uses

ASSISTIVE DEVICES
• 3- or 4-wheeled walker
– e.g., ataxia, hemiparesis, scissors gait
• 2-wheeled walker
– e.g., Parkinson's
• Cane
– Antalgic gait
• Maladaptive devices
– e.g., Don’t use a cane for an ataxic patient

452

hyponatreamia def

Na < 133
determines intravascular volume

453

hyponatremia types and causes

•Hypovolemic hyponatremia:
Diuretics, GI losses (e.g. nausea, vomiting, diarrhea, nasogastric suction), severe
burn wounds, marathon runner, etc.
•Hypervolemic hyponatremia:
CHF, nephrotic syndrome, cirrhosis, excessive IV.
•Euvolemic (90% of all cases):
SIADH, hypothyroidism, Addison's disease
• Pseudohyponatremia:
Hyperproteinemia, hypertriglyceridemia, hyperglycemia.
• Psychogenic: Urine osmolality < 100

454

Hyponatermia treatment

– Acutely altered mental status: 3% saline at 40-50 cc/hr
(<12 mEq/24 hr) adjusting rate to increase Na+ by 0.5-0.6 mEq/hr until symptoms improve
– Hypervolemic: Fluid restriction, diuretics
– Euvolemic: Fluid restriction; treat underlying cause
– Psychogenic: Fluid restriction.
– Hypovolemic: Normal saline
– Pseudohyponatremia: Treat underlying cause

455

Law of consistency: If the pCo2 and HCO3 rise or fall in the same direction and at the rate
expected

(HCO3= [1.1 to 1.3] x pCO2

456

how to correct for hypoalbuminemia in met acidosis

– (Expected albumin – observed albumin) x 2.5 + (observed anion gap) is the
actual anion gap.

457

metabolic alkalosis causes

»likely diuretics, vomiting, hypokalemia (e.g., aldosteronism)

458

creatinine and GFR relationship

inversely

459

Acute Renal Failure causes

1. Pre Renal
2. Post Renal
3. Renal

460

1. Mucous membranes are dry
2. Tenting of the skin- Where?
• Thigh and calf
3. Flat neck veins
4. Orthostatics- Laying/Sitting/standing SBP >20 mm Hg fall,DBP>10 mmHg fall, Pulse
increase of >20
5. Wait 3 min between each maneuver
Fe Na 20/1
1. Volume loss (GI- N-V-D and diuretics)
2. Relative Vol Loss (CHF,Cirrhosis, Nephrosis, Pancreatitis, Burns, etc)
3. Gastro Intestinal Bleed
4. Hypercatabolic state (Prednisone, Sepsis Neoplasia, Burns)
5. TPN

Pre-Renal Azotemia

461

Post Renal ARFCauses

 Obstruction-Acute, Chronic, Complete, Partial
 Hydronephrosis
 Usually takes days to develop or to resolve
 Ultrasound
 Dx- Age related- Reflux,UPJ, Radiation, Prostate cancer, Retroperitoneal Fibrosis

462

 Fe Na > 3
 Bun/Cr < 15/1
 U Na >20
1. No Tenting
2. Normal Membranes
3. Hypotension
4. Could be anything

Renal ARF

463

Renal causes of ARF

 Acute Tubular Necrosis
1. Toxins Vs. Ischemia (hypotension)
2. Oligouric Vs. Non-oliguric ARF
Oliguria ≡ < 400 cc/24 hours
Non-oliguric much better prognostically
Glomerulonephritis
Glomerulonephritis
 Acute- RPGN- Crescent formation
 Chronic
 Primary Idiopathic
 Secondary
 Hypocomplementemic
 Nephritic
 i.e., active urinary sediment with RBCs, etc.
 Nephrotic
 Overlap

464

1. Proteinuria (>3.0 Gms/day)… actually albuminuria
2. Edema
3. Hyperlipidemia ( why?)

Nephrotic syndrome

465

acute interstitial nephritis causes

 Medications- ABX = 71%
 Infection = 15%
 TINU Syndrome (Tissue interstitial nephritis uveitis syndrome) = 8%
 Sarcoidosis = 1%

 Drugs =
Methacillin/PCNs/Cephalosporins/Cimetidine (rare in other H2 blockers)/ Allopurinol/Rifampin
NSAIDS !!!!!!

466

Hyponatremia
 Symptoms- Basically, Altered Mental Status

 Rx- 3% saline at a rate to have serum Na increase by .5 to .6 meq/hr until symptoms improve

467

Again, does not reflect Na stores,rather, total body H20 deficit
Sx = Altered mental status  why?- brain cells “shrink”

Hypernatremia

468

hypernatremia treatment

D5W; NOOOOO Salt!!! (e.g., NS, D5 1/2 NS, D5 1/4 NS)

469

 EKG = “U” waves = prolonged QT interval
 Muscle weakness
 Muscle weakness may be profound; may not be able to walk
 Cardiac Arrest
K+

hypokalemia

treat with K+

470

 K+ 6.0 - 6.5 = Peaked T waves (all leads)
 K+ 6.5 - 7.0 = Loss of P waves (EMERGENCY). Increased PR, wide QRS (>120 ms)
 K+ of greater than 5.5
 Symptoms - same as hypokalemia
 Muscle weakness / cardiac arrest / death
 Acute hyperkalemia is an urgent problem
 Chronic hyperkalemia is not urgent

Hyperkalemia

471

treatment for hyperkalemia

Ca Gluconate immediatley

472

Anion Gap Metabolic Acidosis - MUDPILES

Methanol
Uremia
DKA
Paraldehyde
Isopropyl alcohol
Lactic Acidosis
Ethylene Glycol
Salicylates

473

met acidosis symptoms

 Severe Metabolic acidosis/Resp. Alkalosis
 Stimulation of respiratory center tachypnea
 Altered mental status = “Salicylate Jag”
 Hypokalemia, elevated PT/PTT, hypouricemia, fever
 Tinnitus

474

Treatment for met acidosis

 Alkalinize urine
 Cathartic
 Replace electrolytes
 Dialysis
 Bezoar - 35hr peak levels
 NEVER SEDATE PATIENT

475

Respiratory Acidosis causes

 COPD
 End stage ARDS
 Iatrogenic
 Inability to remove CO2 with ventilation

Turn up O2

476

Respiratory Alkalosis

 Hyperventilation
 Causes- Anxiety, Sepsis, Fevers, Gram negative bacteremia, Iatrogenic, Aspirin toxicity

477

Expected changes between co2 and hco3

 Say HCO3- is 14… 24-14 = 10
 Expected PCO2 would be: 40 – (a range of 1.1 to 1.3) x 10 = 27 to 29. Expected PCO2 should be between 27 to 29. If higher = Respiratory Acidosis; if lower, Respiratory alkalosis

or if C02 is 50, bicarb is 35 to 37

478

4 kinds of kidney stones

calcium - hyperpara,
uric acid - hyperuricemia
cystine
struvite - bacterail enzyme degredation

479

struvite stone tx

remove stone and antibiotic

480

• Generally asymptomatic until stones began to pass into the ureter.
• Pain varies from mild to severe (“worse than childbirth”), and generally develops in paroxysms lasting 20-60 minutes.
• Upper ureteral or renal pelvic obstruction generally causes flank pain; lower ureteral obstruction causes pain radiating to the ipsilateral testicle or labia, and both pain patterns may be present
• Often associated with nausea and vomiting
• Occasionally associated with dysuria and urgency when the stone enters the bladder or urethra

what imaging do you get

noncontrast helical CT scan
ultrasound if preg
urinanalysis
x-ray if calcium stone

481

medical treatment for kidney stone

Encourage fluids for spontaneous passage
Pain control
– Opioids frequently necessary
– NSAIDs fairly effective and may decrease ureteral smooth muscle tone, but might induce ARF and not feasible if vomiting
Strain urine for stone analysis

482

 May occur spontaneously in younger men
 More common after an indwelling Foley catheter
 Fever, chills, dysuria / usually very tender prostate*
 Usually mild pyuria (8-10 WBCs/HPF)
 Positive urine culture more likely following prostate exam


treatment

acute prostatitis

Usually oxyquinolone or third-generation cephalosporin antibiotics x 10 days

483

 Recurrent acute prostatitis symptoms and/or chronic perineal pain and/or chronic dysuria
 Symptoms and rectal tenderness frequently not as pronounced as with acute prostatitis; usually afebrile
 Laboratory findings usually unrevealing
 PSA not infrequently “artifactually” elevated


treatment

chronic prostatitis

 Generally requires at least 12 weeks of oxyquinolone antibiotics

484

 Acute pain and often marked swelling of the epididymis
 May be associated with prostatitis
 Antibiotic treatment as for acute prostatitis
 Usually oxyquinoline or third-generation cephalosporin antibiotics x 10 days
 Warm baths and NSAIDs usually helpful acutely

Acute Epididymitis

485

• Slow urinary stream
• Incomplete emptying
• May have urge incontinence early on and then develop overflow incontinence
 Usually an enlarged slightly firmer prostate on rectal exam
• Possible to have relatively isolated middle / transitional prostate lobe hypertrophy
 Post void residual volume is usually increased

BPH

486

BPH treatments

 Alpha adrenergic antagonists (e.g., doxazosin/Cardura; tamsulosin/Flomax)
• Reduce prostate smooth muscle tone about the prostatic urethra
 5-alpha reductase inhibitors (e.g., finasteride/Proscar)
• Inhibit conversion of testosterone to free testosterone, inducing prosthetic atrophy
 May result in diminished libido and erectile dysfunction
 Usually reduces PSA values by about half; may reduces prostate cancer risk


TURP, TUMP, PSV, TVP TIP

487

 Largely obstructive; may be asymptomatic
 Signs
 Usually a firm nodular mass on rectal exam
• Generally, all nodules must be biopsied
 PSA usually elevated and/or rising
• May be normal (normal values: 0.0-6.2)

Prostate cancer

488

– Hematuria most common, usually painless
– Occasional urgency, frequency and dysuria
• Diagnosis
– Usually by cystoscopic or flexible ureterorenoscopic biopsy
– MRI / CT scan

Bladder or renal cancer

usually transitional cell cancer

489

• Primarily occurs between ages 20-40
– A testicular mass over age 50 is most likely lymphoma
• 2-3 times more likely in an undescended testis
– Orchiopexy prior to puberty reverses increased likelihood
• Symptoms
– Usually a painful testicular mass
• A painless testicular mass is very likely cancer if not clearly a varicocele (bag of worms) or hydrocele (transilluminates)

testicular cancer

490

if BRCA-1 or BRCA-2
– “Too late” if discovered on a pelvic exam
– Ca-125 tumor marker with transvaginal ultrasonography helpful but debatably reliable

ovarian cancer

491

Usually an abnormal vaginal discharge and abnormal vaginal bleeding, especially postmenopausal bleeding

Endometrial uterine cancer

492

how to diagnose and treat

endometrial biopsy
hysterectomy

493

• Increased risk with multiple sexual partners, likely due to HPV (human papilloma virus)
• Diagnosis
– Pap smear / colposcopy

cervical cancer

494

most common organism in UTI

e coli

495

– Urgency, freq, dysuria; occasional hematuria and/or an odiferous urine and/or suprapubic pain
• Diagnosis
– Clinical symptoms; urinalysis and urine culture

Cystitis

3 days of bactrim

496

– Similar to cystitis but may include a vaginal
discharge in females

urethritis caused by chlamydia, gonorrhea and genital herpes

497

– Usually fever, flank pain, nausea and vomiting
– Possible present or antecedent symptoms suggesting lower urinary tract infection
– May lead to sepsis or renal papillary necrosis
• May present as sepsis / septic shock, especially in the elderly and in debilitated and/or demented patients
– Often requires hospitalization, IV fluids and IV antibiotics

pyelonephritis

498

gold standard to diagnose uti

urine culture
get a UA too

499

flank pain and intractable vomiting

kidney stone

500

WBC casts ... what is it and what to do

pyelonephritis --- need hospital and IV antibiotics to avoid septic shock

501

Fatty casts

nephrotic syndorme

502

RBC casts

nephritic syndrome

503

ideal BP for a diabetic

125/75

504

where to aim on xray images

AP - base of 2nd met
lateral - lat cun/cuboid
MO - lateral aspect of 3rd met/cun J
LO - 1st met cun joint
sesamoid - 3rd MPJ
calc - achilles insertion

505

x-rays rapiopaque and radiolucent

•Radiopaque - Bright
•Radiolucent- Dark

506

filter used in podiatry

2.5mm total

507

how many screens used in podiatry

one

508

controls radiographic contrast.

kvp

509

kvp and subject contrast

high kvp = lower subject contract
low kvp = high subject contrast
low kvp increases pateint dose

510

determines the number of x-rays produced

how much used in podiatry

mA
15-30

511

exposure time

1/60sec

512

• Patient dose is therefore a function of

mAs

513

• 15% rule

15% change in KVP is equivalent to 2 times of a change in MA
inversely

514

Inverse Square Law

• Radiation intensity is inversely proportional to the square of the distance from the source

515

common source to image distances

40" or 100cm

516

focal spot sized used in podiatry

1MM

517

greatest tool in keeping patient exposure as low as possible

Collimation

518

Summary
• Moderate to large SID
• Small OID
• Collimate to smallest field of view
• Heel effect ( cathode side for thicker part)
• Grids ( decrease scatter/ increase dose
• Screens ( less x-rays needed)

physics

519

words for bright on xray

Synonyms
Radiopaque
Sclerosis*
Eburnation*

 opaque -- increase in subject density leads to decrease in optical density. Film appears white.

520

words for dark on xray

Radiolucent
Rarefaction*
Osteopenia*
Osteolysis*

 lucent - black areas on film. A decrease subject density leads to increase in optical
density.

521

 Bone apposition on xray

 100% is normal
 0% is dislocated
 Anything between is subluxed

522

m/rems per years for workers

Thus a 20 year old radiology tech is allowed 5 (20-18) which is 10 m/rems per year total body exposure

523

bipartite bones seen

sesamoides
med cun
navicular (rare)

524

anteater signs

CN coaltion

525

Sclerotic halo usually with flat foot

TC coalition

526

os veselanium

off of 5th met base

527

os peroneum

lateral to cuboid

528

os eccentric interphalanges

prox lateral distal phalanx of hallux

529

os naviculare

deeper in TN joint

530

type II accessory navicular

against navicular but not joint

531

growth plate appearances of foot bones

–Base of the phalanges (6 months-3 years)
–Heads of the lesser metatarsals (2 years)
–Base of 1st metatarsal (1 year)
–5th metatarsal base (9-11-years)
–Calcaneus (5 years)
–Tibia (3 months)
–Fibula (6 months)
–Posterior talus (8 years)
–Sesamoids (10 years)

532

primary growth centers are all present at birth except

navicular
cuboid?
lat cun
med cun
int cun
2ry ossification centers

533

apophysis vs epiphysis

• Epiphysis – part of bone that develops separately and then ankyloses.
–Common in tubular bones.
• Apophysis – outgrowth or swelling of bone.
–Tuberosity

534

multiple primary turn into what

bipartites

535

common locations of a pseudoepiphysis

head of 1st met
bases of 2, 3, 4

536

TC coaltion usually seen in 2nd decade and

–Anterior facet – MO
–Posterior and middle – calcaneal axial
–“C” sign
–Talar beaking

537

TN coalition best seen on what view

lateral

538

how does a bone scan work

 Radioisotype (tracer) introduced by IV
 WBC may be tagged to specifically address concerns of infection
 Tracer is delivered via the vascular system
 Tracer attracted to areas of new bone activity/formation
 Localization to hydroxyappetite crystals of the bone matrix
 Tc --A disruption of bone turnover by a pathologic process on the order of 5 to 15% from normal can be detected by bone
scintigraphy - Specificity increases by performing an indium 111-labeled white blood cell test combined with a Technetium-99m-MDP injection.
 A“Geiger”gamma camera counter picks up areas of radioactivity
 Hot spots = Increased Uptake = Dark Areas
 Cold spots = Decreased Uptake = Light Areas
 Photograph taken over time (paper chromatography)
 Cleared by kidneys and excreted in urine

539

most commonly used bone scan radionuclides
why use

tech 99

good marker of inflammation
Good for tumor localization and infection

540

3 phases of a bone scan

Phase I-within 5 min after injection of Tracer – Blood flow phase
Phase II-3-5 hrs post injection - Blood Pool/Inflammatory phase
Phase III –approximately 24 hrs post injection – Delayed phase
6 hr ½life ½

541

WBC labeled

WBCs migrate to areas of infection localization to bone implies a bone infection
Indium-111 labeled WBC, Technetium - 99 labeled WBC (Ceretec) ((HMPAO-Hexamthylpropylamine)
 Pts’ leukocytes are separated out and labeled with indium and reinjected into pt
 hopefully can be used to assist in differentiation between between OM and Charcot
Compare 4 hr tracer to 24 hr tracer, at 24 hrs if tracer still lights up then it is most likely OM

542

bone scan diagnostic value

Any process that induces hyperemic regional blood flow will result in positive in the 1st and 2nd phase
Active bony modeling is positive in 3rdphase
Infection
highly sensitive, but not specific

543

indications for a CT

Imaging of complex structures or pathology
Fractures of Midfoot and Rearfoot
STJ imaging
e.g. tarsal coalitions
Evaluation of malunion/nonunions.
Preoperative workupof Rearfoot and forefoot reconstruction

544

CT potential problems

Metal may degrade image can give“star burst”
Patient has to remain still for up to 30 minutes, may require IV/oral sedation
Issues w/possible claustrophobia - unlikely for foot/ankle

545

MRI is good for

 Inflammation, damage to soft tissue especially ligaments and tendons
 Soft tissue masses, abscesses and osteomyelitis
 Bone lesions (within bone and in cartilage)

546

diff between T1, Spin, T2

 T1 weighted images
 Fat weighted/water suppression
 Fat has high intensity signal (white)
 Short TR (500ms or less)
 Short TE (40ms or less)
 Spin Echo
 “Stir image”- short time inversion recovery
 Water weighted
 Long TR (1500ms or greater)
 Short TE (40ms or less)
 T2 weighted images
 Water weighted/fat suppression
 Water has high intensity (white)
 Long TR (1500ms or greater)
 Long TE (90ms or greater)

547

MRI Danger

1- Small metal objects may move in the magnetic field and cause damage. Pacemakers and Cochlear implants are typically a contraindication to MRI.
2- Torpedo effect- Magnet can pull any metal object in room into the MRI field( pens, scissors, even wheelchairs
3- TATOOS MAY cause minor discomfort to patient during process.

548

Metal implants

High grade stainless steel, titanium, metal alloys may cause artifacts to show up on image causing blurred image

549

muscle on all mri is always

dark grey

550

MRI with contrast

Contrast increases sensitivity to fluid
 E.g. sinus tracts, small abscesses
Gadolinium, Iodinated contrast
Can be placed IV or into a joint

551

tendon disease on MRI

Tendon DISEASE manifests itself as increased signal intensity- representing edema, myxoid degeneration, inflammation or tear.
MRI helps to distinguish acute vs chronic tendonopathy.

552

Magic Angle Effect/ tendon tear Pitfall

Magic angle effect is the phenomenon of anisotropic rotatioin or the 55 degree artifact, giving the false appearance of a tear on T1
On the T2 spin echo dataset, this great signal becomes hypointense and disappears
TIPOFF: the normal appearance of surrounding fat and absence of fluid in sheath
A true Tear is nearly always accompanied by tendon expansion and inflammatory reaction around the tendon

553

Tendon Tear Classification

 0 Hypointense T1/T2
 I. Hyperintense T1, hypointense T2= chronic tear/inflammationor MAE
 II. Hyperintense T1&T2= acute
a. < 50% tendon area (usually hypertrophic)
b. >50% tendon area (hypertrophic or atrophic)
 III. Rupture
a. Supramalleolar
b. Inframalleolar
c. Juxtamalleolar

554

- hyperthyroid induced osteopenia:
- chronic use of anticonvulsant medication:
- deficiency states:
- vitamin-D deficiency: (strict vegetarians, no sun or an extremely low fat diet)
- gastrointestinal and biliary causes;
- renal osteodystrophy
- fibrous dysplasia
BONE NEVER GETS MINERALIZED FROM GET-GO – SOFT BONES

osteomalacia

555

child
Cupping, sclerosis and fraying of metaphysis
Pseudofractures-LOOSER’S LINES
Poorly mineralized epiphyseal centers with delayed appearance
Widening osteoid seams
 osteopenia
Bowing deformities

rickets

556

EXISTING BONE IS DEMINERALIZED/HYPERMINERALIZED
Renal insufficiency and vitamin D deficiency disorders are most relevant
Resultant high PTH leaches out the bone
Medial side demineralization
Sub-periosteal bone resorbtion distal tufts
Periosteal lifting
Ground glass
Lace-like
Vascular calcifications

parathyroid disorders
osteitis fibrous cystica
(browns tumors
calcium replaced with fibrous tissue)

557

DELAYED FUSION OF EPIPHYSIS
DEFORMED OSSIFICATION CENTER/FRAGMENTATION WITH HETEROGENOUS APPEARANCE
SHORT SLENDER SHAFTS OF LONG BONES
DENSE TRANSVERSE BANDS IN METAPHYSIS
WIDE CUPPING OF METAPHYSIS
OSTEOPOROSIS OF METAPHYSIS

cretinism

558

Over 40 male
Increasing hat size
Bone pain
Familial incidence
Chronic build-up and break-down of bone
A-V shunts CHF
Osteosarcoma can result
Flame-shaped lesions/”blade of grass” in long bones
Osteolytic lesions-OSTEOPOROSIS CIRCUMSCRIPTA
Sclerotic bone mixed with lytic bone
Bowed limbs, fail; Fractures, including "banana" or "chalk" transverse fractures
“picture frame” vertebral body

Pagets disease (osteitis deformans)

559

BONE RESORBTION – OSTEOPOROSIS
EXOSTOSES ON LATERAL BORDER OF THE METAPHYSIS-Pelkan Spur
“GROUND GLASS”
INCREASED DENSITY AT METAPHYSIS-Frankel line
SCURVY LINE: lucent line on shaft side of Frankel line
CALCIFICATION OF SUBPERIOSTEAL HEMORRHAGE
WINBERG’S SIGN - sclerotic line surrounding epiphysis

scurvy

560

DECREASED DENSITY IN LONG BONES
TRABECLAR COARSENING
CORTICAL THICKENING
DESTRUCTIVE LESIONS-INFARCTS
MOTTLING-moth eaten
Long slender bones
SALMONELLA OSTEOMYELITIS
PERIOSTEAL NEW BONE-BONE WITHIN A BONE
BRACHYMETATARSIA from infarcts at growth centers
DACTYLITIS with edema

sickle cell

561

ELONGATION & THINNING OF LONG BONES
ARACHNODACTLY
ABNORMAL COLLAGEN

marfans

562

• EXOSTOSIS
• Joint Mice
• Lipping
• “Dorsal Flag”
• Eburnation
• Sub-Chondral
• Sclerosis
• Joint Space Narrowing
• Joint Surface
• Flattening
• Ankylosis
• Arthrodesis
• Heberden’s Nodes
• Bouchard’s Nodes

OA

563

• Juxta-articular Cysts
• Juxta-articular
• Erosions
• Joint Subluxation
• Joint Dislocation
• Osteoporosis
• Osteopenia
• osteomyelitis
• Demineralization

RA

564

• Effusion--Early
• Joint Space Narrowing--Late
• “Punched Out Lesions”
• Overhanging Margins
• Martel’s Sign

Gout

565

• “Fluffy Heel Spur”
• Ankylosing Spondylitis
• Sacroiliitis
• Vertebral Squaring
• SHINING CORNERS
• Syndesmophytes
• Bony Bridging
• Bamboo Spine
• “Fluffy Heel Spur”

Reactive Reiter's

566

• Erosions
• Sacroiliitis
• Terminal Whittling of Proximal Bone
• “Pencil in Cup”
• ARTHRITIS MUTILANS
• Sausage Toe

Psoriatic arthritis

567

Factors to be considered on all chest x-rays include

Inspiration
Penetration
Rotation
Angulation
Orientation

568

Fluffy upper lobe infiltrates
Could be cocci, but can’t make that diagnose on xray

TB

569

airspace disease associated with consolidation (coming together to form a mass).
There is no volume loss.
The air spaces are filled with a water density from the inflammation associated with microorganisms and
pus.
Most common infectious cause of death in U.S

Pneumonia

570

Thin walled cavity think what
Thick

thin - TB, Cocci, WB
Thick -> lung/mass tumor

571

enlarged heart on cxr, what test do you get next

Echo
could be pericardial effusion or cardiomegaly

572

pneumothorax treatment

Treatment is to put on O2 or a breathing tube
Recognize if mediastinum is shifted (Tension

573

SOB, previous DVT
get what test

CT angiography
VQ scan is second but a poor choice

574

COPD signs on chest x-ray

enlargement of retrosternal space and diaphragm flattening

575

CT considerations

Check all menstruating Female pt pregnancy status.
Please note many teens will not be truthful about sexual activity.
CTs irradiate the pt!
•Think twice before ordering.
•Only order when necessary.
•Don’t do imaging without a purpose.
•Know what you’re going to do with the information.
•Will the results change your management?

576

Contra-Indications to IV Contrast

Iodine Allergy
Renal Failure & Not on Dialysis (Based on BUN/Cr and GFR)

577

Foreign Bodies imaging choice

ultrasound

578

Salter Harris Classifications

1 – transverse thru GP
2 – GP and Meta
3 – GP and Epiphysis
4 – GP and Meta and Epiphysis
5 – Crush injury

579

Fracture from FOOSH from normal height

Refer to orthopedic surgeon
Dexa scan if fragility fracture

580

MRI considerations

No metal allowed
Dress in hospital gown
No bras or hair clips
Orthopedic implants ok (except eye for brain)
Welders -> get plain film of orbit!
Most pacemakers and defribillators not allowed
Beware of shrapnel
Closed Scanner -> better image quality, but can cause claustrophobia
Open -> more comfortable but poorer image
30 to 60 mins
Loud noise
400 to 3000 dollars

581

Acute Appendicitis imaging

US in kids
CT in adults

582

Gallstones imaging

ultrasound

583

DVT Dopper things to look for

Compression
Color Flow
Augmentation

584

metastasis to bone
sclerotic and lytic

Sclerotic: Prostate, Lung, Breast
Lytic: Breast, Lung, Renal Cell, Thyroid, MM

585

Complications of pagets

Pathological fractures
2ry Osteoarthritis
Bony deformities
Deafness
Spinal Stenosis
High output CHF
Osteosarcomas

586

how to differ bakers from dvt

Ultrasound
MR if ruptured

587

atlanto-axial subluxation seen in what

rheumatoid

588

avn commonm places

1. Femoral Head
2. Humerus
3. Knee
4. Talus

589

SI involvement
bilateral
syndesmophytes
enthsitis
whiskering
bamboo spine
\

ankylosing spondylitis

590

asymmetry
DIP
early widening of joint
later narrowing
pencil in cup

psoriatic arthritis

591

grading edema

• 0- no edema present
• 1- mild
• 2- moderate
• 3-moderate to severe
• 4-severe

592

• Valleix Phenomenon

– Percussion of the nerve causing proximal and distal radiation or paresthesias

593

muscle strenght testing

0 No muscle contraction is detected
1 A trace contraction is noted in the muscle by palpating the muscle while the patient attempts to
contract it.
2 The patient is able to actively move the muscle when gravity is eliminated.
3 The pt may move the muscle against gravity but not against resistance from the examiner.
4 The patient may move the muscle group against some resistance from the examiner.
5 The patient moves the muscle group and overcomes the resistance of the examiner. This is
normal muscle strength

594

inflammation of vein with blood clot (thrombus) formation (superficial &
deep

thrombophlebitis

595

painless, insidious swelling of the Tissues leadiang to decreased function of the
lymphatic system. May be congenital or acquired

lymphedema

596

Arthritic classes by synovial class

I - non-inflmmatory (OA, ON, Charcot)
II - inflammatory (RA, etc)
III - septic
IV - hemorrhagic
---trauma, PigVillSyn, TB, Neoplasia, Charcot, coagulopathy

597

Class I synovial fluid findings

Clear/yellow
Transparent
WBC < 2,000
<25% pMNs
Culture negative

598

ClassII Synovial findings

Yellow/White
Translucent/opaque
WBC 2,k to 100k
> 50%pMNs
culture neg

599

Class III synovial findings

yellow/white
Opaque
> 100k WBC
> 95% PMNs
Culture positive

600

Class IV synovial findings

Red
Opaque

601

physical findings of OA

firm swelling around joint
crepitus
restricted ROM

602

OA common joints

hips
knees
1st carpal metacarpal joint
1st MTP
PIP, DIP

603

RA common joints

wrists
MCP
ankles
MTP

604

lab tests for RA

high ESR
high CRP'
post rf
pos ccp
anemia

605

ACR criteria for RA

Morning stiffness > 1 hour
4 or more
Arthritis of >3 joint areas
Arthritis of hand joints (MCPs, PIPs, wrists)
Symmetric swelling (arthritis)
Serum rheumatoid factor
Rheumatoid nodules
Radiographic changes

606

extra-articular features of RA

Anemia (most common extra-articular feature)
Nodules – elbows, achilles
Lung disease: fibrosis, nodules, pleural
Cardiac: pericarditis
Vasculitis
FeltySyndrome
Sjogrens syndrome
Lymphadenopathy

607

treatment for RA

-NSAIDS (pros and cons)
-Corticosteroids (lowest dose possible)
-Methotrexate – start at 7.5 or 10mg/week, monitor CBC, Renal, LFT, albumin
-DMARDS

608

Foreign body sensation (sandy or gritty)
Dry or decreased tearing
Burning
Photosensitivity
Itching
Filmy sensation

sjogrens syndrome

609

RA
Splenomegaly
Neutropenia
Other Features
Anemia
Thrombocytopenia
Lymphadenopathy
Leg Ulcers
Skin Pigmentation

Felty Syndrome

610

5 clinical syndromes of Psoriatic arthritis

Asymmetric oligoarticular
Symmetric polyarticular
Arthritis Mutilans
DIP Only
Axial Skeleton

611

definitive diagnosis of gout

“the definitive diagnosis is possible only by aspirating and inspecting synovial fluid or tophaceous material and demonstrating needle shaped monodsoium urate crystals with negative birefringence under polarized microscopy

612

treatment for asymptomatic hyperuricemia

nothing

613

uricosurics

probenicid

614

xanthine oxidase inh

allopurinol (start at 100)
Feuxostat - hepatic glucoronidation
40mg start

615

PMales
over 60
Knee
chondrocalcinosis
often degenerative
Crystalls CPPD
Small rod like
positive birefringence

pseudogout

616

Inflammatory back pain:
Lumbar or buttock pain lasting> 3mo. pg
Alternating buttock pain
Pain worse c rest
Pain improves c activity
Back stiffness> 30 min
Pain awakening pt. in the second half of the night*
Consider what

spondyloarthropathy

617

Seronegative Diseases Share

1. Enthesitis
2 Axial arthritis
3. Peripheral arthritis
4. Tendency toward new bone formation
5. Extraarticular features
6. THE HLA B27 ANTIGEN

618

Prototype of the seronegative spondyloarthropathies
Clear link c HLA Clear link c HLA--B27 mechanism ???
Usually presents c backpain
Male predominance but women do get it (3:1)
Enthesitis -- enthesopathy
Peripheral arthritis
New bone formers
 Extraspinal manifestations:
Eye-acute anterioruveitis
Heart-- aortic insufficiency
Lung--apical disease

ankylosing spondylitis

619

Seronegative asymmetric arthropathy (predominantly lower extremity)
Plusone or more of the following
–– Urethritis/cervicitis
–– Dysentery Dysentery
–Inflammatory eye disease
–– Mucocutaneous disease: balanitis, oral ulceration, keratodermia

reactive arthritis

620

diabetic complications

heart disease
blindness
kidney disease
amputation

621

Tissue changes in diabetes

 Altered protein function and turnover, cytokine activation
 Osmotic and oxidative stress
 Reduced motor and sensory nerve conduction velocity
 Increased glomerular filtration rate and renal plasma flow

622

pedal complications in diabetes

Neuropathy
Vasculopathy
Immunopathy
Limited Joint Motion
Ulcerationi
Infection
Gangrene
Charcot Collapse

623

unholy triad

Neuropathy….….loss of sensation to extremities
Vasculopathy …..decreased blood flow
Immunopathy…..inability to fight infection

624

risk stratification for diabetics

0 - normal - q12 m
1 - PN - q6 m
2 - LOPS, deformity, PAD, q3m
3 - Previous ulcer or amp q1-3m

625

wagner wound classification

 Grade 0: No open lesions
 Grade 1: Superficial Ulcer
 Grade 2: Deep Ulcer
 Involves ligament, tendon, joint capsule or fascia
 No abscess or osteomyelitis
 Grade 3: Deep ulcer with abscess, osteomyelitis, or joint sepsis
 Grade 4: Local Gangrene of forefoot or heel
 Grade 5: Extensive gangrene of entire foot

626

UNIVERSITY OF TEXAS WOUND CLASSIFICATION

Stages
 Stage A: No infection or ischemia
 Stage B: Infection present
 Stage C: Ischemia present
 Stage D: Infection and ischemia present
Grading
 Grade 0: Epithelialized wound/no wound
 Grade 1: Superficial wound
 Grade 2: Wound penetrates to tendon or capsule
 Grade 3: Wound penetrates to bone or joint

627

•‘Pain arising as a direct consequence of abnormalities in the somatosensory system in people with diabetes.’
•A diagnosis of exclusion and is a clinical diagnosis

diabetic neuropathy

628

PN large fiber vs small fiber

Large fiber
▫ Large myelinated fibers (5% of nerves)
▫ Touch, vibratory sense, proprioception
▫ Late finding
▫ Severe disease
▫ Stabbing or shooting symptoms are most common of nerves)


Small Fiber
▫ Unmyelinated and small myelinated nerves (95% f )
▫ Pain, temperature
▫ Earliest finding
▫ Documentable changes precede symptoms
▫ Burning is most common

629

diabetic PN motor neuropathy

Proximal
Amyotrophy-presents with pain, atrophy, and weakness (difficulty standing up, climbing stairs)
Unilateral
Weight loss
Distal
Intrinsic muscle wasting
Hammertoes
Hallux limitus
Equinus

630

= Rapidly reversible sensory symptoms in poorly controlled diabetic patients during episodes of elevated blood sugar.

hyperglycemic neuropathy

631

= Asymptomatic neuropathy becomes temporarily symptomatic with rapid drop in blood sugar

“Insulin Neuritis”

632

PN best prevention tool

normoglycemia

633

therapeutic options for PN

•Symptom Relieving Only
▫ Physical modalities
▫ Antidepressants
▫ Anticonvulsants
•Disease Modifying
▫ Intensive glucose management
▫ Antioxidants/nutriceuticals
▫ Decompression

634

meds used for PN

TCA (amitriptyline)
SNRI (cymbalta, effecxor)
anticonvulsants (gabapentin, Lyrica)
Opiods (tramadol)
Membrane stabilizers (Lidocaine, Mexilitine)
Nutriceutilcals (b-complex, alpha lipoid acid, folate, vit C)

635

Major predisposing factor for DFI is

DF ulcer

636

evidence of infection in DFU

Redness, warmth, swelling, tenderness, or pain
Purulent secretions, undermining of skin edges, foul odor

637

Factors that increase risk of infection:

Probe-to-bone test +, >30 days, recurrent ulcer, PVD
LOPS, renal insufficiency, barefoot walker

638

Clinical Classification of a Diabetic Foot Infection

Uninfected or Grade 1: No signs of infection.
Mild or Grade 2: Locally infected ulcer
Moderate or Grade 3: Foot or limb threatening.
Severe or Grade 4: Life threatening.

639

• Granulation tissue base
• No deep tracts
• No cellulitis
o Most diabetics will respond with cellulitis
• No purulence
o Serous drainage = normal
• Wound lacking purulence or anymanifestation of inflammation.

Grade 1

640

• Presence of ≥2 manifestations of inflammation.
• Cellulitis that extends ≤2cm around the ulcer.
• Infection is limited to skin or superficial subcutaneous tissues.
• No other local complications or systemic illness.

Grade 2

641

• Infection in patient who is systemically well and metabolically stable.
o Has ≥ 1 of the following characteristics:
o Cellulitis extending ≥2cm,
o Lymphangitic streaking,
o Spread beneath the superficial fascia,
o Deep tissue abscess,
o Gangrene,
o Involves the muscle, tendon, joint and/or bone.

Grade 3

642

Signs of a Limb-Threatening Infection

Evidence of systemic inflammatory response
Rapid progression of infection
Extensive necrosis or gangrene
Crepitus on examination
Soft tissue gas on imaging
Bullae, especially hemorrhagic
New onset wound anesthesia
Pain out of proportion to clinical findings
Recent loss of neurologic function
Critical Limb Ischemia
Extensive soft tissue loss
Extensive bony destruction
Failure of infection to improve with appropriate therapy

643

Infection in patient with systemic toxicity or metabolicinstability.
Examples include; fever, chills, tachycardia, hypotension, confusion, vomiting, leukocytosis, acidosis, severe hyperglycemia, or azotemia.

Clinical Classification of a DFI Grade 4: Severe

644

avoid prescribing antibiotic for what

uninfected ulcers

645

when treating DFU as outpatient

Stabilize the patient
In office I&D
Deep tissue culture
Appropriate antibiotic coverage –this may be adjusted on follow up or with culture results
Appropriate shoe wear/off-loading
Appropriate wound care

646

Treatment of Infection -When treating in hospital;

Stabilize patient
Obtain appropriate labs, studies and consults.
Surgical I&D, deep cultures, post-op management and appropriate antibiotics.
Discharge as soon as patient able.

647

if patient had MRSA in past.....

treat them for MRSA

648

common topicals and how long to use

IDSA recommend use for 1-2 weeks only.
Common examples:
Mupirocin
Silver compounds (incl: Silvadene)
Iodine compounds (incl: Betadine)
Gentamicin/Triple Abx preparations
Transition to wound gel once infection controlled

649

IDSA indication for soft tissue infections with oral meds

2-4 weeks of oral antibiotics.
For osteomyelitis: up to 3 months combined therapy.

650

indications for IV antibiotics

Typically reserved for Limb or Life Threatening DFI’s.
Generally started in a hospital setting.
The selection of the antibiotic is often hospital directed.
If MRSA suspected, or patient history, the patient will be empirically covered.
Infectious disease (ID) consults helpful in determining appropriate coverage.

651

mild Staph aurues infection

Keflex
Augmentin (amox/clav)
Clinda

652

mild MRSA infection

Doxycycline
Bactrim

653

moderate staph infection

ampicillin-sulbactam
ertapenem
imipenem

654

moderate to severe MRSA

Vancomycin
Linezolid
Daptomycin

655

Pseudomona infection

mild - quinolones
mod - Pipercillin tazobactam (zosyn) (broad)

656

definitive diagnosis of osteomyelitis

bone biopsy

657

plain radiographs for osteomyelitis

Periosteal reaction/elevation
Loss of cortex with bony erosion
Loss of trabecular pattern or marrow radiolucency
New bone formation
Bone sclerosis with or without erosion

658

 Classic periwound signs
 Brawny edema
 Hyperpigmentation
 Lipodermatosclerosis
 Located in the gaiter (supramalleolar) region
 Irregular borders
 Copious drainage
 Beefy red base
 Painful

venous ulcers

659

 Classic peri-wound signs and symptoms
 Weak pulses/delayed capillary refill
 Skin shiny, atrophic, dry
 Intermittent claudication or rest pain
 Location typically dorsal, distal and over bony prominences
 No drainage
 Pale base
 Black eschar often found
 Very painful

Arterial (Ischemic) Ulcers

660

Classic associated findings
Diminished sensation
Poorly controlled DM
Located plantarly
Round with peri-wound callus and undermining
Painless
Base is variable
Drainage is variable

diabetic ulcers

661

Classic historical findings
Institutionalized patient
Immobile or confined to bed
May have DM, VI, or PAD
Always located over bony prominences
Often painful but not always
Base may be pale/black if ischemic
Often very deep

Pressure ulcers

662

Most common cutaneousmarker of diabetes (present in 40 -50% of diabetic patients)
Sign of increased likelihood of internal complications
Males > females (2:1)
Shins & feet
Round, flat red papules
Fine Scale
Depressed hyperpigmented areas may appear later
Caused by microangiopathy
May be confused with psoriasis (different histopathology) and with NLD (not waxy or shiny)
Rarely symptomatic but may respond to corticosteroid cream (use care in the pretibial region)
Keep skin moisturized
Control blood sugar

diabetic dermopathy

663

Abrupt appearance
Acral location (Acral = away from central trunk)
Porphyrin levels
Immunoflourescence
Intraepidermal
Subepidermal
no hx of trauma

bullosis diabeticorum

664

Clear, non hemorrhagic
Non-inflammed base
Tips of toes and fingers
Long--standing diabetes
Peripheral neuropathy
Good circulation
Heals without scarring
NO HISTORY OF TRAUMA

intraepidermal blisters of BullDiab

665

May be hemorrhagic
Non-inflammed base
Tips of toes & fingers, NWB Areas
Heals with scarringand atrophy
NO HISTORYOF TRAUMA

subepidermal blisters of bulldiab

666

Collagen degeneration w/ granulomatous response
Initial lesion often red or violaceous papule/patch
Lesions enlarge into
-–Sharply demarcated
––Indurated, waxy appearing
–– Depressed or atrophic
–– Yellow-brown plaques
–– Raised borders
–– Telangiectasia common
Most common on shins
Most commonly bilateral
May precede precede the diagnosis of diabetes in 15%
Lesional anesthesia is a hallmark

Necrobiosis Lipoidica (Diabeticorum)

667

considerations for Necrobiosis Lipoidica

malignant transformation (biopsy it)
biopsy

668

treatment of NLD

topical steroids
intralesional steroids