Deck 2 Flashcards
(196 cards)
1
Q
What disease has positive–
- ANA (anti nuclear antibodies)
- Anti histone antibodies
- Anti-dis-DNA antibodies?
A
- Sensitive lupus
- Specific drug induced lupus
- Specific lupus + renal involvement
2
Q
What disease has positive–
1 anti smooth muscle antibodies
2. Mitochondrial antibodies
3. Centromere antibodies
A
- Autoimmune hepatitis
- PBC
- Scleroderma
3
Q
Which disease has positive–
- Anti Ro+La antibodies
- Anti CCP antibodies
- Anti RF antibodies
A
- Sjogrens
- RA
- RA
4
Q
What disease has positive–
- Anti jo antibodies
- Topoisomerase antibodies
A
- Polymyositis
2. Systemic scleroderma
5
Q
Risk factors for heart disease
A
DM Smoking HTN Dyslipidemia Family history Central obesity Cocaine use Sedentary lifestyle
6
Q
What are risk factors for PE
A
Cancer Exogenous hormones Recent surgery Recent immobility including long travel Hypercoagulable states (pregnancy, clotting disorders) History of PE or DVT
7
Q
What is the differential for sharp pleuritic pain?
A
Pneumothorax
Pulmonary embolism
Pericarditis (also positional)
8
Q
What are the life threatening causes of chest pain that you would want to rule out?
A
PE MI Dissection Tamponade CHF Pneumothorax
9
Q
What is the differential for visceral chest pain (aching, poorly localized)
A
Myocardial ischemia
–> worrisome features are prolonged pain of more than 20 min and rest pain
Aortic dissection–abrupt, intense pain (often “tearing”)
10
Q
What is the pathological change behind stable angina and what is its clinical presentation
A
Luminal narrowing
Central chest discomfort worsened by exertion, emotion and eating
Relieved by rest and nitro
11
Q
What is the pathological change behind unstable angina and what is the clinical presentation
A
Plaque rupture or thrombus
Worsening pattern or rest pain
No elevation in troponin, with or without ECG changes of ischemia
12
Q
What is the pathological change behind an NSTEMI and what is the clinical presentation
A
Partial occlusion
Non ST elevation MI–elevation in troponin with or without ECG changes of ischemia
13
Q
What is the pathological change behind a STEMI and what is the clinical presentation?
A
Complete occlusion
ST elevation MI–elevation in troponin, with distinct ST segment elevation in more than two continuous leads, new LBBB or posterior wall MI with reciprocal ST depression in pre cordial leads on ECG
14
Q
What is the cardiac Ddx for chest pain
A
Myocardial–> MI, angina, myocarditis
Valvular–> aortic stenosis–> CHF
Pericardial–> pericarditis, tamponade
Vascular–> aortic dissection
15
Q
What is the pulmonary Ddx for chest pain?
A
Airway–> obstructive (COPD, asthma)
Parenchyma–> pneumonia
Pleural –> Pleuritis, pneumothorax, pneumomediastinum, pleural effusion
Vascular–> pulmonary embolism
16
Q
What is the GI ddx for chest pain
A
Esophagitis Esophageal cancer Gastritis PUD Pyloric stenosis Cholescystitis Pancreatitis
17
Q
Other than cardiac, pulm, GI, what is also on the Ddx for chest pain?
A
MSK –>chostochondritis
Shingles
Anxiety/panic
18
Q
What should you ask for on history for chest pain?
A
- Characterize the chest pain–> location, onset, provocation/palliation, radiation, severity, timing
- Ask about specific patterns of pain for AoD, PE, MI
- Associated symptoms–> dyspnea, palpitations, diaphoresis, syncope, nausea
- Infectious symptoms–> fever chills, headache, fatigue, cough, sputum
- Precipitating factors–> comforting, exertion, trauma
- Meds
- Risk factors for CHD and PE
- ROS–> B symptoms, N/V/D, abdo pain, GU sx
19
Q
What type of process presents typically with mid sternum pain radiating to back, sudden onset, tearing, progressive?
A
Aortic dissection
20
Q
What type of process presents typically with heavy pressure chest pain, retrosternal, comes on suddenly and lasts hours, radiates to arm/jaw/shoulders, and is relieved by nitro?
A
MI
21
Q
What type of process presents typically with pleuritic, sudden onset chest pain that is severe and one sided with dyspnea?
A
PE
22
Q
What signs on physical exam would suggest AoD?
A
- Discrepancy in pulse between arms of more than 20 systolic or more than 10 diastolic
- New aortic regurgitation murmur
- Absent or reduced pulses
23
Q
What does a pericardial rub suggest?
A
Pericarditis
24
Q
What does a new aortic regurgitation murmur on exam indicate?
A
Aortic dissection
25
What does pulsus paradoxus indicate?
More than 10
| Asthma or tamponade
26
What does absent or reduced pulses indicate?
Aortic dissection or emboli
27
What might a new mitral regurgitation murmur indicate in the setting of CP?
Papillary muscle dysfunction secondary to ischemia
28
What does Becks triad indicate? What is Becks triad?
Tamponade
Muffled heart sounds
Hypotension
Elevated JVP
29
What might a loud S2 indicate in the setting of chest pain?
Indicates acute elevation in right sided pulmonary pressure
In the setting of chest pain, suggestive of a PE
30
What does decreased air entry to one side on auscultation of the lungs suggest?
Pneumothorax
31
What might be the pathological process in a patient with chest pain plus:
Hypotension
Elevated JVP
Displaced trachea
Tension pneumo
32
What might be the pathological process in a patient with chest pain plus
Egophony
Decreased air entry
Dullness to percussion
Pneumonia or pleural effusion
33
What might a pleural rub indicate?
Pneumonia or PE
34
Describe a physical exam approach to chest pain
General appearance--apprehension, diaphoresis, pallor, cyanosis, anxiety
Vitals--different BP in arms, pulsus paradoxus, absent or reduced pulses
CV--murmur, pericardial rub, Becks triad, S3, loud S2
Resp--air entry bilaterally, dullness or hyperresonance to percussion, midline trachea, ego phone, pleural rub
Abdo--referred pain or diaphragm irritation
MSK--chest wall tenderness
Skin--zoster
35
What dermatological condition can cause chest pain?
Zoster can cause severe pain before onset of rash
36
What labs should be ordered in the setting of chest pain, and why are you ordering each?
1. Baseline--CBC, lytes, urea, Cr, glucose
2. Cardio--troponin and repeat, BNP
3. Resp--d dimer
4. Infection--CRP, LDH
5. LFTs if indicated by Hx/physical (I.e is suspect referred pain from cholescystitis, etc)
6. ABG--normal ABG does not rule out PE
37
What investigations should be done in the setting of CP and why would you do each?
1. ECG--MI, pericarditis
2. CXR--pneumothorax, pneumonia, CHF
3. Echo--tamponade, valvular disease
4. CT angio--PE (coronary angiography for CAD)
5. VQ scan--PE if patient has kidney disease and cannot tolerate contrast
6. MIBI--ACS
38
What may be components of treatment of any cause of chest pain?
ABC protection
| Cardiac monitor, pulse ox, IV access, O2 provided/made available
39
How would you treat acute MI?
Admit CCU
```
Oxygen
ASA
IV nitro
IV beta blocker
LMWH
clopidogrel
Thrombolysis
angioplasty
Consider GIIb/GIIa inhibitors
```
40
How would you treat unstable angina/ACS?
Admit CCU or monitored bed
```
Oxygen
ASA
IV nitro
IV beta blocker
LMWH
?clopidogrel
?angioplasty
Consider GIIb/GIIa inhibitors
```
41
How would you treat tension pneumothorax?
Admit thoracic surgery
Needle aspiration or thoracostomy
42
How would you treat PE?
Admit medicine or ICU/thoracic surgery
IV/LMWH and oxygen
Directed thrombolysis or consider embolectomy in extreme cases
43
How would you treat cardiac tamponade?
Admit CCU
Pericardiocentesis
44
How would you treat esophageal rupture
Admit ICU/thoracic surgery
Fluids
IV abx
Emergency surgery
45
How would you treat AoD?
Admit ICU or thoracic surgery or Admit CCU
Type A--> ascending aorta
Surgery
Type B--> arch or descending aorta
Medical control of HTN with negative inotropes
Surgery if necessary
46
How would you treat severe pneumonia?
Admit medicine/ICU
IV abx and oxygen
47
How would you treat GI causes of CP including esophageal spasm or reflux
Discharge and follow up with GP
Symptomatic treatment
48
How would you treat a simple pneumothorax
Discharge--follow up in ED for repeat CXR and reassessment
Observe or needle aspiration
49
How would you treat a simple pneumomediastinum
Discharge and follow up as warranted
Observe/investigation of cause
50
How would you treat an uncomplicated pneumonia?
Discharge and follow up with GP
Oral Abx
51
How would you treat pericarditis?
Admit medicine if complicated otherwise discharge and follow up with GP
Treat underlying cause if present
It post viral, NSAIDs and steroids
52
How would you treat MSK/cervical/thoracic radicular causes of CP?
Discharge and follow up with GP
Symptoms treatment
NSAIDs, acetaminophen, adjunctive therapies
53
How would you treat herpes zoster?
Discharge and follow up with GP
Anti virals if lesion onset was within 48-72 hours
Symptom treatment with NSAIDs, acetaminophen, narcotics
54
What are the symptoms of HUS/TTP, DIC?
FAT RN 2
```
Fever
Anemia
Thrombocytopenia
Renal impairment
Neuro impairment
```
2 of the above are required for an immediate smear
55
What can cause folic acid deficiency
Diet or drugs (methotrexate)
56
What pattern on serum iron, TIBC, ferritin would suggest:
| Iron deficiency anemia
Low iron
High TIBC
Low ferritin
57
What pattern on serum iron, TIBC, ferritin would suggest:
| Thalassemias
Normal iron
Normal TIBC
Normal ferritin
In the setting of a macrocytic anemia
58
What pattern on serum iron, TIBC, ferritin would suggest:
| Anemia of chronic disease
Low iron
Low TIBC
High ferritin
59
What pattern on serum iron, TIBC, ferritin would suggest:
| Sideroblastic anemia
High iron
Normal TIBC
Normal or high ferritin
60
What causes pre-renal injuries?
1. True intravascular fluid loss
2. Decreased effective circulating volume
3. Impaired renal perfusion
61
What types of processes cause true intravascular fluid loss?
Blood loss
Renal or GI losses
Inadequate oral intake
Insensible losses (fever, burns)
62
What types of processes cause decreased effective circulating volume?
CHF
Hypoalbuminemia--nephrotic syndrome, cirrhosis, malnutrition
Shock--distributive or cardiogenic
63
What types of processes cause impaired renal perfusion?
1. Macro vascular--> RAS, dissection, thrombus
| 2. Micro vascular--> NSAIDs (afferent vasoconstriction), ACEi (efferent vasodilation), hypercalcemia
64
What are the three areas of the kidney that can be injured causing renal AKI?
Glomerulus
Tubular
Interstitial
Vascular
65
What are the parts of the glomerulus than can be injured in renal AKI?
```
Glomerular capillary wall
Endothelium
Basement membrane
Podocytes
Mesangium
Bowman's space and capsule
```
66
How are glomerular injuries (causing AKI) clinically divided?
Nephrotic syndrome and nephritic syndrome
Can also classify by pathology on renal biopsy and by primary versus secondary
67
What are the clinical features of nephritic syndrome?
1. HTN
2. Active sediment (RBC casts, dysmorphic RBCs)
3. Variable proteinuria (including in the nephrotic range)
4. Oliguria (less than 400 mL per day)
5. Varying renal insufficiency
68
What are the pathological processes behind nephritic syndromes?
1. Linear--> anti glomerular basement membranes disease, Goodpastures disease
2. Immune complex-->
- Primary-->IgA nephropathy, membranoproliferative glomerular nephritic
- Secondary-->SLE, HBV, post strep GN, IE, cryoglobulinemia
3. Pauci-immune (ANCA+ vasculitis)--> GPA (PR3+), MPA (MPO+), EGPA (Churg-Strauss) (MPO+)
69
What are the clinical features of nephrotic syndrome? There is a mnemonic.
PALE
1. Proteinuria more than 3.5 g/day
2. HypoAlbuminemia
3. HyperLipidemia
4. Edema
Also--
Hypercoagulable (loss of protein C and S, anti thrombin)
Immunosuppression (lose immunoglobulin)
Bland sediment (fatty casts, oval fat bodies)
**GFR usually preserved**
70
What are the histopathological classifications of nephrotic syndrome?
Focal segmental glomerulosclerosis
Membranous nephropathy
Minimal change disease
Membranoproliferative GN
71
What are some secondary causes of nephrotic syndrome?
```
DM
Obesity
Autoimmune (SLE, RA)
Infectious (Hep B, C, HIV, EBV, syphilis)
*Drugs (NSAIDs, lithium, heroin)
*Malignancy
```
72
What is RPGN-rapidly progressive glomerulonephritis?
Clinical syndrome manifested by progressive loss of renal function over days/weeks
Must have features of glomerular disease in urine
Often presents as nephritic syndrome of rapid onset
Anti GBM, immune complex, pauci-immune can present as RPGN
73
What are the two types of tubular injuries seen in AKI?
1. ATN
| 2. Intra tubular obstruction
74
What causes ATN?
1. Ischemia--> prolonged pre renal insult
2. Toxic--> drugs (contrast dye, aminoglycosides, acyclovir), pigment (hemoglobin, myoglobin), protein (myeloma light chains)
75
What causes intra tubular obstruction in tubular injury in AKI?
1. Crystals--irate, calcium oxalate, drugs like methotrexate
2. Protein--myeloma light chains
76
How do you distinguish tubular from pre renal AKIs?
1. Rate of rise of creatinine is faster ATN
2. Pre renal will respond to a fluid challenge within the first 24-72 hours
3. The fractional excretion of sodium is less than 1% in pre renal and more than 2% in ATN
4. Urine sodium is less than 20 in pre renal and more than 20 in ATN
77
What are the 5 Is of acute interstitial kidney injuries?
Infection --> bacterial (staph, strep..), viral (CMV, EBV, HIV), fungal
Inflammation --> sjogren's, SLE, IgG4, GPA
Infiltration--> sarcoidosis, TB (usually chronic/progressive), lymphoma
Iatrogenic --> NSAIDs, Abx (penicillins, Sulfa), diuretics, PPI, allopurinol
Idiopathic
78
What is the classic triad of acute interstitial nephritis?
Fever
Rash
Eosinophilia
With or without eosinophils (poor sens and spec)
With or without WBC casts and sterile pyuria
Typically non oliguric (pee normal amount)
79
What types of vascular processes can cause an AKI?
1. MAHAs--> TTP/HUS, malignant hypertension, APLAS
2. Embolic phenomena--> cholesterol, atheroembolic
3. Vasculitis--> PAN, takayasu's
80
What can cause a post-renal injury resulting in an AKI?
1. Urethra--> stricture, stenosis
2. Prostate--> BPH, prostatitis, cancer
3. Bladder--> cancer, stone, clot, neurogenic
4. Ureters-->
- intra luminal--> cancer, stone, clot
- extra luminal--> cancer, pregnancy, retroperitoneal fibroids
81
What are some questions to ask on history to investigate pre renal causes of AKI?
Recent N/V/D/blood loss
Hx CHF, cirrhosis
Use of NSAIDs, ACEi, cocaine
82
What are some questions to ask on history to investigate possible post renal causes of an AKI?
Urinary frequency, urgency, nocturnal, dribbling, hematuria
History of stones, BPH, prostate cancer
Constitutional sx
83
What are some questions to ask on history to investigate a glomerular cause of an AKI? Why would you ask each of them (what are you hoping to rule in or out)?
1. Frothy urine--> proteinuria
2. Hematuria or cola coloured urine
3. Recent URTI/strep throat--> post strep GN
4. Alopecia, oral ulcers, face rash, arthralgias--> SLE
5. Fevers, IE risk factors--> IE
6. History of HBV, HVC or risk factors
7. Family history of GN/IgA nephropathy (especially of Asian descent)
8. Hemoptysis--> pulmonary renal syndromes like GPA
84
What does frothy urine suggest?
Proteinuria
85
What symptoms suggest SLE?
```
Alopecia
Face rash
Oral ulcers
Arthralgias
Renal injury
```
86
What questions would you ask on history to investigate Renal tubular causes of an AKI?
1. Drug history--aminoglycosides, acyclovir, amphoteracin (ATN)
2. Radio contrast exposure (ATN)
3. Gout, malignancy history (urate nephropathy)
4. "Found down" or muscle injury (pigment nephropathy)
87
What questions would you ask on history to investigate renal interstitial causes of AKI?
1. Recent or current infection
2. Drug history --Abx, NSAIDs, diuretics, PPI, allopurinol
3. Rheumatological review of systems (Sjogren's, SLE)
88
What questions would you ask on history to investigate renal vascular causes of AKI?
```
Bloody diarrhea (HUS)
Etc.
```
89
What are some consequences of AKI that you would want to investigate on history?
Symptoms of volume overload--dyspnea, Orthopnea, PND, peripheral edema
Decreased urination--oliguria or anuria
Nausea, malaise, confusion, pleuritic CP (pericarditis), bleeding (uremia)
90
What should you look for in particular on physical exam of the patient with an AKI?
General inspection
Vitals--> hypertension (nephritic syndromes), fevers (IE, pyelonephritis), hypoxemia
Neuro--> orientation, asterixis
H&N--> throat exam (post strep GN), alopecia/facial rash/oral ulcers (SLE)
Respiratory--> crackles (volume overload, pulm hemorrhage)
CV--> JVP, peripheral edema, mucous membranes (volume status--IMPORTANT), new murmur (IE), pericardial rub (pericarditis)
Abdo--> CVA tenderness (pyelonephritis), DRE (BPH, prostate cancer)
Derm--> generalized excoriations, rash (AIN, cryoglobulinemia, vasculitis)
MSK--> arthritis/arthralgias (SLE, gout)
Lymph nodes--> infections and malignancy
91
What investigations would you order to assess an AKI?
1. General
2. UA and micro--> consider urine C&S, urine Na and FENa
3. Renal U/S with or without foley insertion
92
What are the important findings on UA in an AKI?
Proteinuria
Positive heme--> hemoglobinuria, myoglobinuria, hematuria
Positive leukocyte esterase--> pyelonephritis or AIN
93
If you see Uric acid crystals on urine microscopy, what disease are you thinking
Uric acid nephropathy
94
If you see calcium oxalate on urine microscopy, what are you thinking?
Ethylene glycol poisoning
95
If you see dysmorphic RBCs on urine microscopy what are you thinking?
Glomerulonephritis
96
If you see isomorphic RBCs on urine microscopy what are you thinking?
Stones, malignancy, IgA, TBMD
97
If you see no RBCs on urine microscopy but positive heme on dipstick, what are you thinking?
Hemoglobinuria from TTP/HUS or myoglobinuria from rhabdomyolysis
98
If you see WBCs on urine micro, what are you thinking?
Infection
| Interstitial nephritis
99
What do hyaline casts indicate on urine micro?
Common and NON SPECIFIC
Can be a sign of volume depletion
100
What do RBC casts indicate on urine microscopy?
Glomerulonephritis
101
What do WBC casts indicate on urine micro?
Interstitial nephritis
| Pyelonephritis
102
What do heme granular casts indicate on urine micro?
"Muddy brown casts"
ATN
103
What do fatty casts indicate on urine micro?
Found with significant proteinuria like in nephrotic syndrome
104
What does a FeNA of less than 1% indicate?
Tubules are still functioning and reabsorbing sodium
Pre renal cause of AKI
105
What does a FeNA or more than 1% indicate?
Sodium not being maximally resorted
ATN or non volume depletion cause
106
What's the best way to determine if you patient has a pre renal AKI?
Fluid challenge
107
Tests for SLE
ANA
C3
C4
108
Tests for post infectious strep
ASOT
109
Tests for IE
Blood cx
110
Tests for cryoglobulinemia
Crayons
| HCV
111
Tests for membranoproliferative glomerulonephritis
HBV
HCV
HIV
112
Tests for anti-GBM disease
Anti GBM antibody
113
Tests for GPA, MPA, Churg Strauss
ANCA
114
Tests for multiple myeloma
SPEP and UPEP
115
What are the 5 golden rules of AKI management?
1. Give fluids if dry--> pre renal management
2. UA and micro--> renal investigation
3. Stop nephrotoxic drugs, really dose meds--> all causes
4. Insert foley--> post renal management
5. Order renal U/S to rule out hydro--> post renal suspicion
116
What are the acute indications for dialysis? There is a mnemonic.
AEIOU
Acidosis--> refractory metabolic acidosis
Electrolytes--> refractory hyperkalemia
Ingestion--> methanol, ethylene glycol
Overload--> refractory volume overload
Uremia--> pericarditis, encephalopathy, asterixis, seizures
117
What is the basic diagnostic approach to AKIs?
Pre renal
Renal
Post renal
118
What is the basic process of AKI evaluation and work up
Hx, Physical, Basic labs
UA and micro
Fluid challenge
Insert foley and get renal U/S
Stop nephrotoxic drugs and renal dose meds
Evaluate for acute indications for dialysis (AEIOU)
119
What is normal body temp?
36.8 +/- 0.4 degrees
120
What is defined as fever?
Higher than 37.2 in AM
Higher than 37.7 in PM
121
What is the definition of fever of unknown origin? What are the types?
More than 38.3 on several occasions over a defined period with us revealing investigations
1. Classic--> lasting more than 3 weeks, where 3 outpatient visits, 3 days in hospital or 1 week of ambulatory testing revealed no cause
2. Nosocomial--> 3 days of investigations and 2 days of Cx with no growth
3. Neutropenic--> 3 days of investigations and 2 days culture with ANC less than 0.5
4. HIV associated
122
Define fever and state the physiological changes fever causes
Elevation of body temp with elevation in hypothalamic set point
Causes peripheral vasoconstriction--> patient feels cold
Heat production mechanisms are activated--> shivering
Nonspecific myalgias and arthralgias
123
What is hyperthermia and how does it differ from fever
Increased body temp not due to pyrogens (no increase in hypothalamic set point)
124
What is the Ddx of classic FUO?
Infection
Neoplasm
Inflammatory disease--> systemic rheum disease, vasculitis, granulomatous disease
Misc--> PE, drug fever, hereditary fever syndrome, hypothalamic dysregulation
125
What is the Ddx of nosocomial FUO?
```
Infection (catheter, c diff, sinusitis)
No infectious (drug fever, PE, cholescystitis)
```
126
Ddx of neutropenic FUO
More than 60% of patients with febrile neutropenia are infected and 20% are bacteremic
Candida and aspergillosis are common
127
Ddx of HIV associated FUO
More than 80% are infected
128
What should you be asking about on Hx in a patient with FUO
```
Particular attention to chronology
Meds
Pet exposures
Sick contacts
Sexual contacts
Travel
Trauma
Malignant symptoms
```
129
What should you focus on in physical exam in a patient with FUO
General complete physical exam looking for infectious or malignant symptoms
Precise rash description if present
130
What should you order in terms of investigations for FUO
```
CBC and diff
Lytes
BUN/Cr
LFTs
ESR/CRP
UA
Infectious workup--> HIV, CMV, EBV, TB skin test, VDRL
Autoimmune--> ANA, RF
Cultures--> urine, blood, sputum
Malignant--> SPEP, UPEP
If indicated by sx--> CXR, AXR
```
131
How do you treat FUO?
Treat underlying cause
Antipyretics--> aspirin, NSAIDs, glucocorticoids
If patient is hyperpyretic use cooling blankets
132
Name some agents commonly associated with drug induced fever
```
Allopurinol
Captopril
Erythromycin
Heparin
HCTZ
Isoniazid
Nifedipine
Penicillin
Phenytoin
Procainamide
Quinidine
```
133
What is the most common cause of decreased renal function in hospitalized patients
Pre renal
134
Why do you get elevated urea in pre renal AKI
Enhanced tubular absorption of both sodium and water increases passive reabsorption of urea
135
What is the most common type of intrinsic renal failure?
ATN
136
What is the leading cause of intrinsic renal injury in hospitalized patients
Sepsis
Next most common is renal ischemia during major heart surgery or vascular surgery
137
What is the most common cause of acute interstitial nephritis
Allergic reaction to drug
Look for fever, drug rash, eosinophilia or renal dysfunction
Commonly fluoroquinolones, Sulfa drugs, beta lactams, NSAIDs
138
How does NSAID associated interstitial nephritis usually present
As nephrotic syndrome
139
How do ACEi cause renal injury?
Efferent vasodilation which causes decrease in filtration pressure
140
What drugs are know to cause efferent arteriole vasoconstriction in the kidney
Amphoteracin B
Cyclosporine A
NSAIDs
Radio contrast
141
What types of cells and casts will be seen in ATN
Renal tubular epithelial cells
Granular and muddy brown casts
142
What type of cells and casts will be seen in acute glomerulonephritis
Dysmorphic RBCs
RBCs
WBCs
Epithelial cells
RBC
143
What types of cells and casts are seen in acute interstitial nephritis (AIN)
Eosinophils
WBCs
WBC and hyaline
144
What are the symptoms of hypercalcemia
Bones, stones, groans, moans, psychiatric overtones + dehydration
Bone pain
Kidney stones
Abdo pain
Psych presentation
Dehydration because hypovolemic because calcium is an active osmole
145
How do you treat hypercalcemia
1. Fluids--make them pee it out, works right away
2. Treatment for malignant hypercalcemia is bisphophonates like PAMINDRONATE once you have normalized the calcium level (inhibit osteoclasts resorption of bone)
3. Imaging to work up mets if malignant
Loop diuretics increase calcium excretion and work right away
Calcitonin SC can inhibit bone resorption and works within hours
Surgery for primary hyperparathyroidism
146
Describe and approach to hypercalcemia
Either high PTH or low PTH then go from there
147
What is the Ddx of hypercalcemia with low PTH
1. MALIGNANCY--> breast, lung, colon, kidney, prostate and multiple myeloma
- -on Hx ask about risks for these cancers
2. Vitamin D excess
3. Thiazides
4. Milk alkali syndrome
5. Increased bone turnover states--> ie Paget's disease
148
What is the Ddx of hypercalcemia with high PTH?
1. HYPERPARATHYROIDISM
Primary versus tertiary--> tertiary is in renal patients that have had high PTH for so long that is becomes autonomous
2. Familial hypocalciuric hypercalemia (FHH)--> don't pee out calcium
149
What is the mechanism behind malignant hypercalcemia
1. Lytic lesions
2. Paraneoplastic (produces PTH related peptide)
3. Increased conversion of inactive to active vitamin D
150
How does PTH increase serum calcium
By activating bone resorption and increasing renal tubular resorption of calcium
Also increases activation of vitamin D which assists in increasing calcium resorption from the gut
151
What does calcitonin do?
Produced by thyroid parafollicular C cells
Acts to reduce serum calcium through inhibiting bone resorption
152
What is the definition of hypercalcemia
Corrected serum calcium of more than 2.6 mmol/L
*for every decrease of 10g/L in albumin, correct serum calcium by adding 0.2 mmol/L
153
What are the mechanisms of hypercalcemia
```
Increased bone destruction
Decreased renal excretion
Increased GI absorption
Unregulated secretion of PTH
Vitamin D abnormalities
```
154
What causes primary hyperparathyroidism
Parathyroid adenoma
Parathyroid hyperplasia
Parathyroid carcinoma
155
What ingested substances can cause hypercalcemia
```
Increased vitamin d
Vitamin D intoxication
Thiazide diuretics
Lithium intake
Milk alkali syndrome
```
156
What to ask on history for hypercalcemia
```
Fatigue
Anorexia/weight loss
GI complaints
Bone pain
Tobacco use
Drug ingestion
Excess vitamin ingestion
```
157
What do you look for on physical exam for hypercalcemia
Usually unrevealing
| Look for signs of malignancy (adenopathy, masses)
158
What labs should you order in the hypercalcemia workup
```
Intact PTH assay
Ionized Ca
Mg
Phosphate
ALP
Vitamin D
Lytes
Urea
Cr
```
```
If likely malignant-->
CXR
Urine for red cells (renal cancer)
Mammogram
SPEP and UPEP
CT if no cancers yet found after above
```
159
Symptoms of hypocalcemia
```
Peri oral paresthesias
Tingling of fingers and toes
Tetany
Stridor (laryngospasm)
Seizures
Confusion
Weakness
Meds (loop diuretics, bisphophonates, calcitonin, anticonvulsants)
```
160
What changes might you see on ECG in hypocalcemia
Long QTc
| ST changes
161
How do you manage hypocalcemia
If severe symptoms--> CALCIUM GLUCONATE 1-2 amps slowly push IV then run calcium drip and MgSO4 drip over 4 hours
If mild symptoms--> calcium carbonate 1-2 g PO TID or QID with calcitriol PO
*treat underlying cause
162
Causes of hypocalcemia
1. PTH related--> low PTH, high phosphate
- hypoparathyroidism (surgery, radiation, autoimmune, congenital, infiltrative)
- functional hypoparathyroidism (hypomagnesemia)
2. PTH resistance--> pseudo hypoparathyroidism
3. Non PTH related
- vitamin D abnormalities (will have high PTH) I.e nutritional, malabsorption, altered metabolism (cirrhosis, renal failure, anticonvulsants)
- drugs (phosphate infusion causing hyperphosphatemia, calcitonin, loop diuretics)
- hungry bone syndrome
- acute--> acute pancreatitis, rhabdomyolysis, tumour lysis, toxic shock syndrome
- other--> calcium malabsorption, hypoalbuminemia
163
What organs are important in vitamin D metabolism/conversion?
Liver and kidney
164
What does vitamin D do
Increases ca reabsorption in gut, kidney and bone
Increases phosphate reabsorption at gut and kidney
Decreases PTH
165
What does PTH do?
Increases calcium reabsorption at distal tubule and bone
Decreases phosphate absorption at proximal tubule
Increases vitamin D
166
What is the respiratory Ddx for dyspnea
1. Airway--> COPDE, asthma exacerbation, acute bronchitis, infectious exacerbation of bronchiectasis, foreign body obstruction
2. Parenchyma--> pneumonia, interstitial lung disease acute exacerbation, ARDS
3. Vascular--> PE, pulm HTN
4. Pleural--> pneumothorax, pleural effusion
167
What is the cardiac Ddx for dyspnea?
1. Myocardial--> HF exacerbation, MI
2. Valvular--> Aortic stenosis, acute aortic regurgitation, mitral stenosis, endocarditis
3. Pericardial--> pericardial effusion (tamponade)
4. Vascular--> CAD (ACS, stable angina)
168
What are the systemic Ddx for dyspnea
Anemia
Sepsis
Metabolic acidosis
169
What are some non-cardiac/resp/systemic causes of dyspnea
Neuromuscular (can't expand chest wall)
Psychogenic
Anxiety
170
What causes of dyspnea present with:
1. Sputum production
2. Cough
3. Pleuritic chest pain?
1. Bronchitis, pneumonia, COPD
2. Chronic bronchitis, asthma, pneumonia, airway irritation
3. PE, spontaneous pneumothorax, pneumonia
171
What causes of dyspnea present with:
1. Visceral chest pain
2. Hemoptysis
1. Heart failure
| 2. PE, bronchitis, pneumonia
172
What should you ask about on HPI for dyspnea?
Cough
Sputum production
Pleuritic or visceral chest pain
Hemoptysis
Risk factors--> smoking (COPD, bronchitis), cardiac Hx (HF), occupational or enviro exposures (asbestos, tire factory, dust)
Baseline fitness and change from baseline
173
What causes of dyspnea may present with
1. Wheeze
2. Strider
3. Consolidation/dullness to percussion
1. Asthma, heart failure, COPD
2. Upper airway obstruction
3. Pneumonia
174
What causes of dyspnea may present with
1. Crackles/rales, S3, high JVP
2. Cardiac murmur
3. Tracheal shift from midline
1. HF
2. Valvular disease
3. pneumothorax
175
What causes of dyspnea may present with
1. Leg swelling or pain
2. Hyper expansion
3. Fixed split S2, loud pulmonic component of S2, RV heave, JVP increased
1. DVT--> PE
2. COPD
3. Pulm HTN
176
What are signs of hyperexpansion seen in COPD?
Less than 4 cm tracheolaryngeal height
Barrel chest
Reduced cardiac dullness to percussion
Distant heart sounds
177
What labs and investigations should be ordered in the setting of dyspnea?
```
CBC, lytes, urea, Cr
Troponin
Calcium, magnesium, phosphate
BNP if suspect HF
D dimer/CT PE if suspect PE
Sputum gram and culture
ECG (most common finding in PE is sinus tachy)
CXR--> pneumothorax, pneumonia (consolidation), HF (pleural effusions, Kerley B lines, batwinging, peri bronchial cuffing)
Spirometry (FEV1/FVC)
ABG if in acute resp distress
Echo for valvular disease
```
178
What tools can you use in assessing a possible COPDE
BODE index
| GOLD classification
179
What is the BODE index
BMI, Obstruction, Dyspnea, Exercise
Scoring system and capacity index used to test patients who have been diagnosed with COPD and predict long term outcomes for them
180
What is the GOLD classification
Scoring system for COPD
Based on degree of airflow limitation measures with PFTs
Stages I--> IV are mild to severe
181
What are COPDE triggers
```
Infection
Pollutants
Non-adherence
PE
Pulmonary edema
Pneumothorax
COPD progression--natural course
```
182
What is a normal FEV1/FVC?
70-85% (meaning most people blow out 70-85% of their inspiration in the first second of a forced vital capacity expiration)
183
How does emphysema differ from the other lung diseases on PFTs
Increased TLC (same on everything else)
184
How does interstitial lung disease differ from the other lung diseases on PFTs
Decreased residual volumes (the others have increased residual volume)
185
How do you manage COPDE acutely?
1. ABC--> keep O2 sat above 90% or between 88-92% if they are a CO2 retainer, establish IV access
2. Bronchodilators--> salbutamol and ipratropium
3. Steriods--> prednisone 40-60mg PO daily x 5-14 days (or methylprednisone IV)
4. Abx--> give if any two of the following are present--> increased sputum prurulence, increased dyspnea or increased sputum volume --> consider lexofloxacin if no renal disease, doxycycline, amoxicillin, cefuroxime or azythromycin
5. Consider need for BiPAP, intubation
NPPV--> initiate early if mod/severe dyspnea, acidosis, increased PaCO2, RR higher than 25 as it results in 58% less intubation a and decreases length of stay and mortality
Intubation if--> PaO2 less than 55-60 mmHg, increasing PaCO2, decreasing pH, increased RR, respiratory fatigue, change in mental status, or hemodynamics instability
6. DVTP, chest physio
186
How would you treat COPD long term?
Mild or moderate--> short acting inhaled bronchodilator PRN or standing inhaled bronchodilator (LAA better than LABA)
Severe or very severe--> inhaled corticosteroid + LAA and/or LABA
```
Smoking cessation in everyone
Vaccinations in everyone
Consider pulmonary rehab
Consider theophylline
Home O2 as indicated
```
187
Define hyperkalemia
K higher than 5 mmol/L
188
Symptoms of hyperkalemia
Muscle weakness
| Cardiac--> tall peaked T waves, wide QRS, wide and flat p wave, VF
189
What are the causes of hyperkalemia?
1. Pseudo hyperkalemia--> hemolysed blood sample, leukocytosis, thrombocytsis
2. Increased intake --> rare
3. Shift out of cells--> metabolic acidosis, diabetes (insulin deficit), beta blockade
4. Increased release--> rhabdomyolysis, tumour lysis, strenuous exercise, intravascular hemorrhage
5. Decreased output--> decreased distal renal tubular flow (renal failure, decreased effective circulating volume), hypoaldosteronism (decreased renin, adrenal insufficiency, renal tubular acidosis, ACEi, ARBs, spironolactone, NSAIDs)
190
What labs would you order in a patient with hyperkalemia
```
CBCD, lytes, urea, Cr, glucose
CK--rhabdomyolysis?
Serum osmolality
UA
Urine lytes
Urine osmolality
```
Calculate trans-tubular K gradient (TTKG)--> (Kurine x Osm-serum) / (Kserum x Osm-urine)
ECG
Hypoaldosteronism workup--> serum aldosterone and plasma renin activity
Rule out hemolysis and tumour lysis--> haptoglobin, LDH, peripheral smear, bili
Rule out shift--> acidemia
If GFR normal, consider decreased distal Na delivery and urine flow
191
How do you treat hyperkalemia
Treat the underlying cause
In acute situations, must treat the hyperkalemia
**more than 6.5 mmol/L is an emergency**
1. Stabilize membranes--> calcium gluconate
2. Shift K+ into cells--> insulin (with glucose/D5), B agonists (albuterol), bicarbonate (exchanges K for H within cells)
3. Promote K+ excretion--> diuretics to make them pee and kayexalate to make them poo it out
192
Define hypokalemia
Less than 3.5mmol/L
193
Differential for hypokalemia
Decreased intake
Increased shift of K into cells (beta agonism)
Increased losses
- Renal--> diuretics, renal tubular defects, hyperaldosteronism (increased mineralocorticoids)
- GI--> vomiting, NG suction, hypomagnesemia
194
What are the symptoms of hypokalemia
```
N/V
Ileus
Weakness
Muscle cramps
Rhabdomyolysis
Polyuria
```
Cardiac--> arrhythmia, sinus Brady or junctional tachy, AV block, VT, VF
ECG--> U waves, ventricular ectopic, ST depression, small T waves
195
Investigations for hypokalemia
```
CBC
Lytes
Urea
Mg
Glucose
CK
Serum osmolality
UA
Urine lytes
Urine osmolality
```
196
How do you manage hypokalemia
1. Replace K-> KCl 10mEq in 100mL D5W bolus x3, continuous infusion max KCl concentration is 40mEq/L
2. K supplement--> K-dur 20-120 mEq PO divided over once daily to QID--> oral preferred over IV in general
3. Treat underlying cause
