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1

Symptoms of hyponatremia

Usually related to water shifts from brain (cerebral edema) --> lethargy, confusion, coma, seizures

2

Hyponatremia values

<135mmol/L

3

H. Pylori infection treatment

PPI (lansoprazole) + 2 antibiotics (usually clarithromycin + amoxicillin) for 14days

4

Common causes of hypervolemia

Congestive heart failure
Cirrhosis
Nephrotic syndrome

5

Common treatment for hyponatremia

Diuretics

6

Most common cause of euvolemic hyponatremia

Syndrome of inappropriate ADH

7

Aortic dissection

Tear in intima to allow false lumen through media

8

ABG
Ph/pco2/po2/hco3

7.4/40/100/24

9

Causes of low albumin

Liver disease (ie cirrhosis)
Renal disease
Malnutrition

10

NT associated with Parkinson's

Dopamine

11

COPD

Progressive airflow limitation associated with abnormal inflammatory response to noxious stimulants

12

2 main branches of COPD

Chronic bronchitis
Emphysema

13

Symptoms of ICP

Headache
Nausea
Vomiting
Papilledema

14

Advil

Ibuprofen

15

Tylenol

Acetaminophen

16

Aspirin

Acetylsalicylic acid

17

Possible causes of pulmonary embolism

Endothelial injury (ie. surgery)
Stasis (ie. pregnancy)
Hypercoagulation

18

Diastolic murmurs

Aortic regurgitation
Mitral stenosis

19

Systolic murmurs

Mitral regurgitation
Aortic stenosis

20

COPD patient

Blue bloater

21

Most prominent spinous landmarks

C7 (most prominent when neck is bent)
T7 (at level of spinous tip)
L4 (at level of iliac crests)

22

Pulsus paradoxus

Abnormally large decrease in systolic BP with inspiration (ie. >10mmHg)
Related to cardiac tamponade, COPD, constrictive pericarditis, chronic sleep apnea, croup, asthma

23

Negative inotropes

Weaken heart contraction

24

Positive inotropes

Strengthen heart contraction

25

Acetylcholine

Parasympathetic NS neurotransmitter

26

Most common cause of low PaO2/low O2 sat

V/Q mismatch (parts of lung that are getting perfused but not ventilated OR parts of lung that are getting ventilated but not perfused)

27

Most common cause of post-operative V/Q mismatch

Atelectasis

28

Total body water makes up __ of body weight

60%

29

Total body water distribution

2/3 ICF
1/3 ECF (3/4 interstitial, 1/4 plasma)

30

Ratio of replacement of blood loss with crystalloid solution

3:1

31

Ratio of replacement of blood loss with colloid solution or blood

1:1

32

CHFe

Forgetting meds
Anemia, arrhythmia, acidosis
Infection, infarction, iatrogenic
Lifestyle
Upregulators (cocaine)
Rheumatic... valvular dz
Embolism

33

Causes for AG metabolic acidosis

MUDPILES
-Methanol, Metformin
-Uremia
-DKA, EtOH ketoacidosis, starvation ketoacidosis
-Phenformin, Paraldehyde
-Iron, isoniazid, inhalants (cyanide, carbon monoxide)
-Lactic acidosis
-Ethylene glycol
-Salicylates

34

Compensation for acute respiratory acidosis

For every 10 increase in CO2, bicarb rises by 1

35

Compensation for metabolic alkalosis

For every 1 increase in bicarb, PCO2 increases by 0.7

36

Compensation for metabolic acidosis

For every 1 drop in bicarb, PCO2 drops by 1.2

37

Compensation for acute respiratory alkalosis

For every 10 decrease in CO2, bicarb decreases by 2

38

Compensation for chronic respiratory acidosis

For every 10 increase in CO2, bicarb rises by 4

39

Compensation for chronic respiratory alkalosis

For every 10 decrease in CO2, bicarb decreases by 4

40

Typical angina includes all 3 of

1. Retrosternal chest pain
2. Exacerbated by stress/emotion
3. Relieved by nitro/rest

41

Atypical angina includes

2 of:
1. Retrosternal chest pain
2. Exacerbated by stress/emotion
3. Relieved by nitro/rest

42

Non-cardiac chest pain includes

0-1 of:
1. Retrosternal chest pain
2. Exacerbated by stress/emotion
3. Relieved by nitro/rest

43

Classes of angina

I. CP with strenuous exertion
II. CP with walking >1flight of stairs or >2 blocks on flat ground
III. CP with walking <1 flight of stairs or <2 blocks on flat ground
IV. CP at rest

44

Unstable angina includes

ONE OF:
1. rest angina
2. New onset angina (CCS > III within 2 months of initial presentation)
3. Increasing angina (increased by at least 1 CCS class within 2mo of presentation to at least CCS III)

45

Trop repeat at

3-6h

46

STEMI tx

B-MONA
B = Beta-blockers (decrease HR)
M = Morphine
O = oxygen
N = Nitroglycerin
A = ASA + anti-coagulation (Heparin or enoxaparin)
+ high-dose statin
Get PCI, CABG, thrombolytics

47

STEMI dx

ECG and clinical context
Do not wait for trop
Get PCI catheterization ASAP (within an hour) or thrombolysis or CABG if non-PCI hospital then transfer to get PCI

48

NSTEMI dx

ECG, cardiac biomarkers
If low risk (TIMI 0-2) --> exercise MIBI for perfusion
If high risk (TIMI >3) --> early catheterization within 24-48h

49

TIMI

Risk score for all-cause mortality and morbidity of UA/NSTEMI:
Age >/= 65
>/= 3 CAD risk factors (ie. HTN, dyslipidemia)
Known CAD (stenosis >/=50%)
ASA in past 7d (still had angina in spite of ASA)
Severe angina (>/=2 episodes in 24h)
EKG ST changes
Positive cardiac biomarker

50

Long-term prevention for myocardial recovery

ASA, STATINS, ACEi, BB
- ASA and statins lifelong
- ACEi and BB for at least 1y
Dual antiplt therapy after stent placed (~1y, minimum 1mo for metal stent)
*drug-eluting stent needs longer

51

Lateral leads represent

Left circumflex artery

52

Antero-septal leads represent

LAD artery

53

Inferior leads represent

Right coronary artery

54

Absolute C/I to thrombolysis (6)

Hx of intracranial hemorrhage
Ischemic stroke past 3 mo
cerebral malformation or tumour
Possible aortic dissection
Bleeding diathesis
Significant head trauma in the past 3mo

55

Relative C/I to thrombolysis (10)

BP > 180/110
Ischemic stroke >3mos
Dementia
Traumatic prolonged CPR (>10mins)
Major surgery in past 3wks
Internal bleeding past 4 wks
Non=compressible vascular puncutres
Pregnancy
Warfarin
Prev use of fibrinolytic

56

Aortic stenosis

Early-late peaking systolic murmur (crescendo-decrescendo)

57

Aortic regurgitation

Early diastolic or holo-diastolic murmur, blowing

58

Mitral stenosis

Low-pitched mid-diastolic rumble with opening snap

59

Medications for mitral stenosis

Negative chronaotropic agents and HR control (BB and CCB)

60

Mitral regurgitation

Holosystolic murmur over apex

61

EtOH Hepatitis

AST:ALT = 2:1
GGT elevated
IgA elevated
Ferritin elevated
That N

62

AI hepatitis

ASMA +
ANA +
ALKM + (in children)
Very high bill, ALT and AST
High GGT, ALP
IgG elevated

63

Wilson's

Ap7B mutation
Low ceruloplasmin
High 24h urine copper

64

Wilson's tx

Chelation with penicillamine
Maintenance with zinc

65

Hemochromatosis

C282Y or H63D
Increased ALT, AST
Increased T-Sat
Increased ferritin

66

Hemochromatosis tx

Phlebotomy
Regular monitoring
Avoid Vit C
Chelation with deferoxamine (last line)

67

NAFLD

General transaminitis

68

NAFLD tx

Weight loss, fatty!

69

PBC

Intra-hepatic only
Classic picture = young female
Very increased bill, GGT, ALP
Increased ALT, AST
Increased IgM
AMA +

70

PBC tx

Urodeoxycholic acid (UDCA)
Transplant

71

PSC

Intra and extra-hepatic (no clear b/w for dx)
Increased bili, AST, ALT
Very increased GGT, ALP
ANCA +
Associated with IBD (UC > Crohn's)
IgG4 high

72

PSC tx

ERCP for strictures
Transplant

73

Negative inotrope examples

BB
CCB
Class IA antiarrhythmic agents (procainamied)

74

Positive inotrope examples

Digoxin
Amiodarone
Calcium
Catecholamines - Dobutamine, epinephrine, norepinephrine
PDEi - Milrinone

75

Orthostatic hypotension

Decrease in systolic blood pressure of 20 mm Hg or a decrease in diastolic blood pressure of 10 mm Hg within three minutes of standing when compared with blood pressure from the sitting or supine position.

76

Protease affected in TTP

ADAMTS13

77

Classic pentad of TTP

Thrombocytopenia
MAHA
Renal failure
Fever
Mental status change

78

Main tx for TTP

PLEX (plasma exchange) - replace ADAMTS13

79

Classic triad HUS

MAHA
Thrombocytopenia
Acute renal failure

80

TTP: Hx, puts, smear, fibrinogen. INR/PTT

Hx: Drugs, HIV, pregnancy, malignancy, diarrhea, AI disease
Plts: Low
Smear: Many schistos, large plts
Fibrinogen: Normal
INR/PTT: Normal

81

DIC: Hx, puts, smear, fibrinogen. INR/PTT

Hx: sepsis, trauma. malignancy, obstetrical complications
Plts: Low
Smear: Fewer schistos, large plts
Fibrinogen: low
INR/PTT: high

82

Thrombocytopenia

Plts <150 000/uL

83

HUS

Commonly a/w shiga-toxin producing E. coli

84

DIC

Damage to endothelium --> release of tissue factor --> triggering of coagulation cascade = thrombosis

85

Only possible cause of single digit platelet levels

Immune thrombocytopenia

86

ITP first line tx

Steroids (prednisone) for ~4wks

87

ITP second line tx

IVIG
Rituximab
New TPO agonists
Splenectomy
Rhogam in Rh+ pts

88

Type I HIT (heparin-induced thrombocytopenia)

Mild thrombocytopenia within first 2 d of starting heparin but returns to normal while on heparin

89

Type II HITT (heparin-induced thrombocytopenia with thrombosis)

Usually within 5-10d after exposure
ABs target heparin + PF4 complex --> immune complex that aggregates platelets = thrombocytopenia and thrombosis

90

HITT tx

Stop heparin
Alternate anticoagulant (danaparoid, bivalrudin, argatroban) until plts back to normal, then switch to warfarin with 5d overlap

91

PTH function

1. Increases reabsorption of Ca2+ at distal tubule and bones
2. Increases reabsorption of PO4 at proximal tubule
3. Increases calcitriol

92

Drugs a/w hypercalcemia

Vit D toxicity
Thiazide
Lithium
Tamoxifen
Tums

93

Symptoms of hypercalcemia

Moans - Abdo pain from constipation, pancreatitis, PUD, N/V
Groans - bony pain
Stones - kidney stones
Psychiatric overtones - delirium

94

Tx of hypercalcemia

1. IV NS fluids
2. If >3mmol/L, bisphosphonates (ie. pamidronate, zoledronate)
3. Maligancies -- prednisone, calcitonin
4. Dialysis if kidneys can't handle it
5. Denosumab (monoclonal antibody against RANK-L)

95

Role of calcitriol

1. Increases Ca reabsorption in gut, kidney, and bone
2. Increases PO4 reabsorption at gut, kidney
3. Decreases PTH

96

Salbutamol

Ventolin
SABA

97

Ipratroprium bromide

Atrovent
SAMA

98

Lateral leads

I, aVL

99

inferior leads

II, III, aVF

100

Anteroseptal leads

V1, V2

101

Anterior leads

V3, V4

102

Anterolateral leads

V5, V6

103

NSTEMI ECG findings

ST-depression
T-wave inversion or flattening

104

Wellen's sign

T-wave inversion or biphasic T-waves in V2-V4
Highly specific for critical stenosis of LAD

105

HFrEF

EF >40% --> systolic HF

106

HFpEF

EF > 40% --> diastolic HF

107

Systolic dysfunction

Impaired contractility - MI, ischemia, chronic volume overload, dilated cardiomyopathy
Increased after load - Aortic/pulmonic stenosis, systemic/pulmonary HTN
Non-ischemic causes - drugs/toxins, hyper/hypothyroid, infection, infiltration, postpartum EtOH

108

Diastolic dysfunction

Impaired relaxation - LVH, hypertrophic obstructive cardiomyopathy or restrictive cardiomyopathy, MI
Obstruction to filling - mitral/tricuspid stenosis, pericardial constriction, tamponade

109

NYHA classification of HF

I - CHF symptoms with strenuous exercise
II - CHF symptoms with >2 flat blocks or 1 flight of stairs
III - CHF symptoms with <2 flat blocks or 1 flight of stairs
IV - CHF symptoms at rest

110

Why CHFe now?

F - forgetting to take regular meds
A - anemia
I - Infection, ischemia (MI)
L - Lifestyle changes (diet, exercise)
E - endocrine (hyper, hypothyroid), Et,OH
D - drugs (NSAIDs, steroids)

111

EHS in systolic heart failure

S3

112

EHS in diastolic heart failure

S4

113

BNP sensitivity vs specificity

BNP is a highly SENSITIVE test (if negative it is good for ruling OUT)
Not as specific b/c if positive, it may be CHF but lots of other things also cause high BNP (ie. PE, PHTN, LVH, AFib)

114

5 key CXR findings in CHF

1. Increased cardio thoracic ratio (Cardiomegaly)
2. Vascular redistribution
3. Kerly-B lines
4. Peri-bronchial cuffing
5. Pleural effusions and/or pulmonary edema

115

BNP results

<100 = unlikely HF
100-250 = compensated LV dysfunction
250-500 = Diastolic and systolic dysfunction
500-1000 = Decompensated
>1000 = severe HF

116

CHF acute tx

LMNOP
IV lasix
Morphine/monitoring
Nitro (not really needed in right-sided HF)
Oxygen
Positioning upright

NO BETA BLOCKERS

117

CHF chronic tx (triple therapy)

ACEi/ARBs (decrease RAS contribution)
BB (decrease sympathetic contribution)
Spironolactone (decrease RAS/aldosterone contribution)

118

Non-drug therapies for HF

1. Implantable defibrillators - class II/III CHF and EF < 35% on max medical therapy
2. Cardiac resynchronization therapy - class III/IV and QRS >120 ms on max medical therapy
3. LVAD/heart transplant

119

FEV1/FVC dx for COPD

<70%

120

TLC dx for restrictive lung disease

<80%

121

Ascites

(1) Increased hydrostatic pressure (ie. CHF, portal vein thrombosis, cirrhosis, budd chair)
(2) Decreased oncotic pressure (ie. malnutrition, liver disease, nephrotic syndrome)
(3) Increased capillary permeability/lymphatic obstruction (ie. infections (SBP), malignancy, pancreatitis)

122

SAAG

Serum albumin - ascites albumin
If > 11 = portal HTN (cirrhosis, HCC, etc)
If < 11 = non-portal HTN cause (peritoneal carcinomatosis)

123

Spironolactone : Lasix ratio

5:2

124

Tx for acetaminophen overdose

NAC - produces glutathione which is used to turn NAPQI into non-toxic metabolites
Acetaminophen --> NAPQI (toxic) --> non-toxic metabolites

125

SBP features

Ascites white count > 500
Ascites fluid pH <7.4
Ascitic protein <1g/dL
Positive gram stain and C&S

126

SBP microbiology

E. Coli > Klebsiella > Streptococcus pneumoniae
(usually mono microbial, if poly microbial then consider GI perforation)

127

SBP tx

2nd or 3rd generation cephalosporin for 5d (ie. Ceftriaxone of Cefotaxime)
IV albumin

128

Type I hepatorenal syndrome

Rapid onset, prognosis of 2-3 months
More serious

129

Type II hepatorenal syndrome

Gradual onset, prognosis of 6-9 months

130

Hepatorenal syndrome pathophysiology

Liver failure --> NO/prostaglandin release --> systemic (including splanchnic) vasodilation --> decreased ECV -->
--> RAAS activation (renal constriction) --> BUT not enough to counter splanchnic vasodilation) = pre-renal failure

131

Hepatorenal syndrome dx

Cirrhosis with ascites
Cr > 133
Lack of improvement in Cr 48h after diuretics stopped and volume expansion with albumin IV for at least 2 d
No other cause for renal impairment
Absence of intrinsic renal disease

132

Hepatorenal syndrome tx

Raise SVR (ie. NE)
Stop diuretics
Give fluids, albumin
Octreotide (somatostatin analogue which counters vasodilator release)
TIPS = transjugular intrahepatic portosystemic shunt

133

Pancreatitis causes

I GET SMASHED
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps and other viruses (EBV, CMV, HIV)
AI disease (SLE, polyarteritis nodes, pregnancy)
Scorpion stings
Hypertriglyceridemia, hypercalcemia, hypothermia, hypotension (ischemic)
ERCP, emboli
Drugs (SAND + MR VET)
- Sulphasalazine
- Azathioprine
- NSAIDs
- Diuretics
- Metronidazole
- Ranitidine
- Valproate
- Erythromycin
- Tetracyclines

134

Transudative causes of pleural effusion

SYSTEMIC illness (low protein, oncotic vs hydrostatic pressure imbalance)
- HF, hypoalbuminemia (cirrhosis, malnutrition, nephrotic syndrome), SVC obstruction, atelectasis, trapped lung, peritoneal dialysis, PE

135

Exudative causes of pleural effusion

LOCAL disease (high protein, local factors influence fluid clearance)
- PE, malignancy, infection, CT disease, hypothyroidism, hemothorax, inflammatory (pancreatitis, ARDS), abdominal fluid (ascites, pancreatitis, abscesses near lung)

136

Light's Criteria - transudative vs exudative source of pleural effusion

Fluid is exudative if ONE of the following Light's criteria is present
- Fluid serum total protein ratio >0.5
- Fluid serum LDH ratio > 0.6
- Fluid LDH > 2/3 ULN

137

Microvascular complications of diabetes

Neuropathy
Nephropathy
Retinopathy

138

Macovascular complications of diabetes

CVD
PAD
CAD

139

Insulin titration for DKA

Insulin bolus of 0.1/kg
Then insulin maintenance of 0.1/kg/h
Try to keep glucose decline at 3-5mmol/L/hr

140

Key features of HHS (Hyperosmolar hyperglycaemic state)

Glucose VERY elevated (>33.3, usually >40)
Serum osmolality VERY elevated (>320)
No or minimal ketones (no ketoacidosis)

141

Typical DKA patient

Young, T1DM

142

Typical HHS patient

Older, T2DM

143

Main form of tx for HHS patients

Fluids
Requires less insulin to close AG

144

Rapid acting insulin

Humalog (Insulin lispro)
NovoRapid (Insulin aspart)

145

Short acting insulin

Humulin-R
Novolin ge Toronto

146

Intermediate acting

Humulin-N
Novolin ge NPH

147

Long-acting basal insulin analogues

Insulin detemir (Levemir)
Insulin glargine (Lantus)

148

Pre-mixed insulin

Humulin
Novolin
Humalog
Novo Mix

149

Drugs associated with SIADH

SOMA
S = SSRIs
O = Opioids
M = MDMA
A = Anti-convulsants

150

Calculating serum osmolality

(2x Na) + Glucose + BUN

151

SIADH causes

Pain, nausea, anxiety, stress
Cancer - SCLC, pancreatic, duodenum, thymoma, lymphoma
Lung dz - TB, abscess, pneumonia, viral pneumonitis
CNS - trauma, infection
Drugs

152

Na+ correction in hyperglycaemia

Add 3 to serum [Na] for every 10mmol/L of glucose above normal

153

Cause of hyperosmolar hyponatremia

Hyperglycemia

154

Expected urine osm and urine Na in hypo-osmolar causes of hyponatremia

Urine osm > 500
Urine Na < 20 (Aldo NOT working)

155

Expected urine osm and urine Na in low effective circulating volume/hypervolemic causes of hyponatremia

Urine osm >100
Urine Na <20 (Aldo IS working)

156

Expected urine osm and urine Na in SIADH

Urine osm >100 (often >300)
Urine Na >40 (Aldo not affected b/c euvolemic state)

157

Disease associated with rapid correction of hypovolemic hyponatremia

Osmotic demyelination syndrome

158

Definition of hypernatremia

Serum Na+ > 145mmol/L

159

Treatment for central diabetes insipidus

ADH

160

Euvolemic causes of hypernatremia

* Neurogenic
* Trauma, tumours, infections (meningitis, TB, encephalitis), infiltrative (sarcoidosis), vascular, idiopathic
* Nephrogenic
* Renal disorders (polycystic kidneys, infiltration, infection, ischemia), hypercalcemia, medications (lithium)
* Diabetes insipidus

161

Heparin antidote

Protamine

162

Octreotide

Somatostatin analogy - lowers portal venous pressure

163

Labetolol

Alpha 1 and beta 1 and 2 blockers

164

Nitroprusside

Use in hypertensive urgency/emergency
Affects arterial and venous dilation

165

Hydralazine

Arteriolar dilator

166

Secondary causes of HTN

CNS
Hyperthyroid
OSA
Aortic coarctation
Adrenals - pheo, cushings, hyperaldo
Renal

167

Causes of renal artery stenosis

Atherosclerosis
Aneurysm
Fibromuscular dysplasia
Vasculitis

168

When to switch to SC insulin

pH > 7.3, HCO3 >15
AG closed
Pt tolerating normal diet

169

Na+ correction in hyperglycaemia

Increase Na+ by 3 for every 10mmol/L increase in glucose above normal

170

Pericarditis ECG findings

ST elevation diffuse across all leads
PR depression
PR elevation in aVR

171

Ischemia ECG findings

ST depression and/or T-wave inversion in the anatomic territories

172

RBBB ECG findings

Wide QRS in most leads
RSR' in V1/V2

173

LBBB ECG findings

Wide QRS in most leads
Notched R-wave in V5/V6

174

Right-sided leads

V1, V2

175

Left-sided leads

V5,V6

176

1st degree AV block

Increased PR interval >200ms
PR interval constant

177

2nd degree AV block, Mobitz Type I

Progressively increasing PR interval leading to failed conduction
Associated with AV node disease

178

2nd degree AV block, Mobitz Type II

Constant PR (either normal or prolonged) with random failures
Associated with His-Bundle disease

179

3rd degree AV block

Wide QRS
No impulse through --> P waves and QRS at own pace
Block can be at AV node, His bundle, Purkinje, etc.

180

LVH ECG findings

1. Sum of S-wave in V1 and R-wave in V5 or V6 (larger of two) >/=35mm
OR R-wave in lead aVL >/= 11mm
2. +/- strain = ST depression and/or T-wave inversion in I, AVL, V4-V6

181

RVH ECG findings

1. Pre-dom R wave in V1 (> 7mm)
2. R-wave may get progressively smaller from V2-V4
3. Deep S-waves in V5-V6
4. +/- strain in V1-V3

182

Causes of secondary hypertension

Head down approach:
Head/CNS: Pituitary tumour causing acromegaly
Neck: Hyper/hypothyroid, OSA, hyperparathyroidism causing hypercalcemia
Chest: Coarctation of the aorta, aortic dissection
Renal: Renal parenchymal disease (chronic renal failure, polycystic kidney disease, glomerulonephritis), renal artery stenosis
Adrenal: Pheochromocytoma, conn's syndrome, cushing's syndrome
Drugs: NSAIDs, corticosteroids, anabolic steroids, OCP, cocaine, amphetamines, MAOI, SNRI, SSRI, cyclosporine, tacrolimus

183

Hyperaldosteronism workup

Serum renin/aldosterone
Hypokalemia

184

Pheochromocytoma workup

24h urine metanephrines

185

Cushing's workup

24h urine cortisol
1mg dexamethasone suppression test
Late night salivary cortisol

186

Renovascular workup

Renal doppler US
CT/MRI angiogram
Renal angiogram

187

Medication not used first line for its >/=60 y.o. due to falls risk

Beta blocker

188

Medications with proven mortality benefit for hypertension

ACEi and Chlorthalidone (diuretic)

189

If poor BP control on trip or quadruple therapy, consider...

Alpha adrenergic blockers
Centrally acting agents
Aldosterone antagonists
Vasodilators (hydralazine, nitrates)

190

HTN drug combos to avoid

ACEi and ARB
Diltiazem and Metoprolol (Non-DHP CCB and BB)

191

First line agents for HTN in pt with stable angina

BB
Long-acting CCB
ACEi

192

First line agents for HTN in pt with recent ACS

BB
ACEi/ARB

193

First line agents for HTN in pt with decreased LVEF

ACEi/ARB
BB
Nitro/hydralazine
Aldosterone antagonists

194

First line agents for HTN in pt with non-diabetic CKD

ACEi/ARB
Thiazide
Loop for volume control

195

First-line agents for HTN in pt with diabetes without nephropathy

ACEi/ARB or thiazide or ND-CCB

196

First line agents for HTN in pt with diabetes with nephropathy

ACEi/ARB then ND-CCB

197

CCB dyhydropyridine

Potent vasodilators
Ex. Nifedipine, amlodipine, felodipine

198

CCB non-dihydropyridine

HR control
Ex. Verapamil, diltiazem

199

S/E of thiazides

Hypokalemia, hyponatremia, worsening gout

200

S/E of ACEi/ARBs

Hyperkalemia, renal failure

201

S/E of CCB DHP

Peripheral edema

202

S/E of CCB non-DHP

Bradycardia, confusion

203

S/E of BB

Fatigue, ED, bradycardia, depression

204

Hypertensive emergency

sBP >/= 220 and/or DBP >/= 120 with end organ damage (pulmonary edema, MI, renal failure, papilledema, fundoycopic hemorrhages or exudates, hypertensive encephalopathy, CV hemorrhage or stroke, aortic dissection)
Loewr BP in mins/hours using IV agents (Labetolol or nitroprusside/nitroglycerin IV) then oral agents (Captopril, labetolol, clonidine, hydralazine)

205

Hypertensive urgency

Lower BP over 24h with oral agents (ie. Lasix 20-40mg PO x1 dose)
Other options: Captopril, Labetolol, Clonidine, Hydralazine
Lower BP over hours to days b/c if too rapid there's risk of stroke or MI

206

Late systolic murmur

Mitral valve prolapse

207

Aortic valve murmur radiation

Carotids

208

Pulmonic valve murmur radiation

Left shoulder

209

Tricuspid valve murmur radiation

xiphoid right of sternum

210

Mitral valve murmur radiation

Axilla

211

AKI

Increase in Cr by 26umol/L in 48h OR 1.5x baseline OR <0.5cc/kg/h UO

212

Causes of nephritic syndrome

Anti-GBM (Good Pasture's)
IgA Nephropathy
Membranoproliferative glomerulonephritis
Secondary to SLE, HBV, HCV
Pauci-immune

213

Nephrotic syndrome proteinuria

>3.5g/d

214

Causes of nephrotic syndrome

Focal segmental glomerulosclerosis
Membranous nephropathy
Minimal change disease
Membranoproliferative GN
Secondary to DM, obesity, AI, Infectious, drugs (NSAIDs, lithium, heroin), malignancy

215

Clinical feature of nephrotic syndrome

PALE
Proteinuria (>3.5g/d)
hypoAlbuminemia
hyperLipidemia
Edema
+ hyper coagulable state (lose protein C&S and antithrombin), immunosuppression (lose immunoglobulins)
GFR usually preserved

216

2 causes of ATN

Ischemic (pre-renal causing renal)
Toxic (drugs - acyclovir, ahminoglycosides, contrast, pigment, myoglobin, protein)

217

Casts seen in pre-renal causes

Hyaline

218

Casts seen in nephritic syndrome

RBC

219

Casts seen in nephrotic syndrome

Fatty casts/oval bodies

220

Casts seen in ATN

Muddy brown casts

221

Causes of acute interstitial nephritis

Infection (bacterial, fungal viral)
Inflammation (Sjogren's, SLE, IgG4)
Infiltration (sarcoidosis, TB, lymphoma)
Iatrogenic (PANDA - PPI, abx - penicillins/sulfa, NSAIDs, diuretics, allopurinol)
Idiopathic

222

Trio of AIN

Fever
Rash
Eosinophilia
+/- urine eosinophils and WBC casts

223

Vascular causes of renal AKI

MAHA
Embolic
Vasculitis

224

Functional excretion of Na+

(Urine Na+/Plasma Na+) / (Urine Cr/Plasma Cr)
If <1% - kidneys still functioning well to reabsorb Na+ = pre-renal
If >1% - kidneys not reabsorbing, so issues are ATN or non-volume depletion ethology

225

AIN or pyelonephritis casts

WBC

226

Urine osmolality based on pre-renal vs renal

Pre-renal: Uosm >500
Renal: Uosm 250-300

227

SLE special tests to order

C3, C4, ANA, anti-dsDNA

228

Post-infectious causes of AKI special tests to order

Anti-streptolysin O Titre

229

IE special test to order

Blood cultures

230

Membranoprolifer glomerulonephritis special tests to order

HBV, HCV, HIV

231

Anti-GBM disease special tests to order

Anti-GBM antibody

232

Pauci-immune

MPA (microscopic polyangiitis)
GPA (granulomatosis with polyangiitis)
EGPA (Eosinophilic granulomatosis with polyangitis OR Churg-strauss

Tx: IV pulse steroids followed by PO steroids with PO cyclophosphamide for 1 y

233

Pauci-immune special test to order

ANCA

234

Multiple myeloma special test to order

SPEP/UPEP

235

Pre-renal urinalysis, BUN/Cr, FENa, urine osmolality, urine sodium

Hyaline casts
20:1
<1%
>500mOsm
<20

236

Renal urinalysis, BUN/Cr, FENa, urine osmolality, urine sodium

Abnormal casts (RBC, fatty, muddy brown/heme granular)
<20:1
>1%
250-300mOsm
>40

237

Indications for dialysis

AEIOU
Acidosis (refractory metabolic acidosis)
Electrolytes (refractory hyperkalemia)
Ingestion (methanol, ethylene glycol, ASA, lithium)
Overload (refractory volume overload after tx with lasix)
Uremia (pericarditis, encephalopathy, asterixis, seizures)

238

Azotemia

High levels of nitrogen-containing compounds in the blood (ie. urea, Cr)

239

Minimal change disease

T-cell abnormality causing increased glomerular permeability
Primary or secondary (NSAIDs, Li, interferon, NHL, Hodgkin's, leukaemia, HIV)
Tx: Steroids, cyclophosphamide, cyclosporine

240

Membranous glomerulonephropathy (MGN)

Pure nephrotic
Causes: primary or secondary (solid tumours, hodgkin's SLE, RA, syphillis, HBV, HCV)
Glomerular BM thickens in parts causing it to be leaky to proteins
Tx: Steroids, cyclophosphamide, cyclosporine, tacrolimus

241

Membranoproliferative glomerulonephritis

50% nephrotic (type 1), 30% acute nephritic (type 2)
Type 1 = immune complex deposited in kidney
Type 2 = activation of complement system (C3)
Causes: primary, secondary type 1 (HCV, HBV, endocarditis, abscess, SLE); secondary the 2 (sickle cell, complement deficiency)
Tx: steroid, cyclophosphamide, cyclosporine

242

Focal segmental glomerulosclerosis

More severe form of MCD
Pure nephrotic

243

Anti-GBM nephritis

Antibody against alpha-3 chain of type IV collagen
Nephritic
vs Good pasture's which also affects lung
Tx: PLEX, PO steroids and PO cyclophosphamide for 1yr

244

IgA nephropathy

IgA immune complexes deposit in mesangium
Primary vs secondary (celiac, dermatitis, herpes, cirrhosis, HIV, malignancy)
Mostly nephritic< <10% nephrotic
Tx: ACEi to slow progression, steroids, cytotoxic agents
20-40% end up with ESRD over 20y

245

Alpha-1 receptors

Peripheral vasoconstriction = increased PVR
Tx for sepsis
1st line --> NE (alpha-1 agonist)

246

Beta-1 receptors

Inotropic and chronotropic effect = increased CO
Tx for cardiogenic shock
1st line --> Dobutamine

247

1st line tx for anaphylactic shock

Epinephrine

248

1st line tx for cardiogenic shock WITH pulmonary hypertension

Phosphodiesterase inhibitor (Milrinone)

249

qSOFA

2/3 of:
BP < 100 systolic
Altered mental status
RR >22 breaths per minute

250

SIRS

>/2 of:
Temp >38.3C or <36C
HR > 90BPM
RR > 20
PaCO2 <32mmHg
WBC >12 or <4

251

Sepsis

SIRS + infection

252

Anemia

<135g/L in men
<120g/L in women

253

Microcytic anemia ddx

MCV <80uL
TAILS
Thalassemia
Anemia of chronic disease
Iron deficiency anemia
Lead poisoning
Sideroblastic anemia

254

Iron deficiency anemia

Low iron
Low ferritin
High transferrin (TIBC)
Low TSAT

255

Increasing iron absorption

Vitamin C
Meat/fish

256

Thalassemia dx

Target cells on smear
Narrow RDW, smaller MCV than Fe deficiency
Less profound anemia
Normal iron studies
Hb electrophoresis

257

Anemia of chronic disease

-Decreased response to EPO
-Hepcidin (acute phase reactant from liver) causes decreases Fe absorption from gut and decreased Fe release from macrophages and bone marrow
-Cytokines also influence above

258

Retic count

Normal = 1%
Appropriately compensated anemia = 3-10%

259

Tx for iron def anemia

Oral or parenteral iron
PO 1st line = Ferrous sulphate 65mg
Other PO: Ferrous fumarate 106mg, ferrous glauconite 28-36mg
IV options: iron sucrose, iron dextran, ferric gluconate complex

260

Anemia of chronic dz dx

Normal or high ferritin
Low Fe
Low TIBC (diff from Fe-def)
Normal or low TSat
Low relic

261

Anemia of chronic dz tx

Treat underlying disease
May need EPO for CKD
Iron replacement NOT needed

262

Lead poisoning blood smear

Microcytic hypo chromic anemia with basophilic stippling

263

Sideroblastic anemia

Impaired heme biosynthesis and increased cellular Fe uptake

Increased TSat
Decreased transferrin
Increased ferritin
Fe overload!

264

Acquired causes of sideroblastic anemia

EtOH
Drugs (isoniazid, chloramphenicol, linezolid, Copper deficiency, zinc toxicity, hypothermia)

265

Normocytic anemia

MCV 80-100
Retic count high --> hemolysis, hemorrhage or treated nutritional deficiency
Retic count low --> BM problem or non-BM problem

266

AI hemolytic anemia

Warm-agglutins (IgG) - AI causes
Cold-agglutins (IgM)
DAT + - Infectious causes

267

Non-immune causes of hemolytic anemia

Sickle cell, spherocytosis, elliptocytosis
G6PD or PK deficiency
Blood toxins/infections like malaria
Vascular issues like abnormal valves, vasculitis, HUS/TTP/DIC, HELLP

268

G6PD deficiency

Inability to reduce glutathione --> RBCs unable protect themselves from oxidative damage/stress

269

Pyruvate kinase deficiency

Inability for RBCs to produce ATP so membrane pumps stop working and cell dehydrates and lyses

270

Normal BM but low retic normocytic anemia

TACE
Toxins
Anemia of chronic disease
CKD
Early Fe deficiency

271

Abnormal BM and low retic normocytic anemia

BM failure (aplastic anemia)
Infiltration (Heme - myeloma, indolent lymphoma, myelofibrosis, MDS; non-heme - solid tumour, infection, inflammatory)

272

Microcytic anemia

MCV >100
Megaloblast + = Vit B12/folate deficiency
Non-megaloblast + --> BM Normal or abnormal?
If BM normal = HALT
Hypothyroidism
Alcohol
Liver disease
Toxins
If abnormal BM - MDS, myeloma, indolent lymphoma

273

Warm agglutinins tx

Treat underlying disease
Steroids
Consider splenectomy or immunosuppressants
Transfuse with caution

274

Cold agglutinins tx

Avoid cold

275

Hemolytic anemia b/w

Bili high
LDH high
Haptoglobin low
Retics high
Smear - spherocytes (AI), schistocytes (MAHA)

276

High protein states peripheral smear (ie.multiple myeloma)

Rouleaux

277

Cold agglutination peripheral smear

Agglutination

278

Warm agglutinins peripheral smear

Spherocytes

279

G6PD deficiency peripheral smear

Bite cells

280

Thalssemia peripheral smear

Target cells

281

Iron deficiency peripheral smear

Pencil cells

282

Uremia peripheral smear

Burr cells

283

MDS, megaloblastic peripheral smear

howell jolly body

284

ECG of hyperkalemia

Tall tented T-waves (first sign)
Loss of P-wave (atrial paralysis)
Widening QRS (conduction abnormalities)
QRS continues to widen, approaching to sine wave (