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Internal Flashcards

1
Q

Symptoms of hyponatremia

A

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

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2
Q

Hyponatremia values

A

<135mmol/L

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3
Q

H. Pylori infection treatment

A

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

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4
Q

Common causes of hypervolemia

A

Congestive heart failure
Cirrhosis
Nephrotic syndrome

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5
Q

Common treatment for hyponatremia

A

Diuretics

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6
Q

Most common cause of euvolemic hyponatremia

A

Syndrome of inappropriate ADH

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7
Q

Aortic dissection

A

Tear in intima to allow false lumen through media

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8
Q

ABG

Ph/pco2/po2/hco3

A

7.4/40/100/24

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9
Q

Causes of low albumin

A

Liver disease (ie cirrhosis)
Renal disease
Malnutrition

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10
Q

NT associated with Parkinson’s

A

Dopamine

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11
Q

COPD

A

Progressive airflow limitation associated with abnormal inflammatory response to noxious stimulants

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12
Q

2 main branches of COPD

A

Chronic bronchitis

Emphysema

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13
Q

Symptoms of ICP

A

Headache
Nausea
Vomiting
Papilledema

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14
Q

Advil

A

Ibuprofen

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15
Q

Tylenol

A

Acetaminophen

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16
Q

Aspirin

A

Acetylsalicylic acid

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17
Q

Possible causes of pulmonary embolism

A

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

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18
Q

Diastolic murmurs

A

Aortic regurgitation

Mitral stenosis

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19
Q

Systolic murmurs

A

Mitral regurgitation

Aortic stenosis

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20
Q

COPD patient

A

Blue bloater

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21
Q

Most prominent spinous landmarks

A

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

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22
Q

Pulsus paradoxus

A

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

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23
Q

Negative inotropes

A

Weaken heart contraction

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24
Q

Positive inotropes

A

Strengthen heart contraction

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25
Q

Acetylcholine

A

Parasympathetic NS neurotransmitter

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26
Q

Most common cause of low PaO2/low O2 sat

A

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

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27
Q

Most common cause of post-operative V/Q mismatch

A

Atelectasis

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28
Q

Total body water makes up __ of body weight

A

60%

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29
Q

Total body water distribution

A

2/3 ICF

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

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30
Q

Ratio of replacement of blood loss with crystalloid solution

A

3:1

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31
Q

Ratio of replacement of blood loss with colloid solution or blood

A

1:1

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32
Q

CHFe

A 
Forgetting meds
Anemia, arrhythmia, acidosis
Infection, infarction, iatrogenic
Lifestyle
Upregulators (cocaine)
Rheumatic... valvular dz
Embolism
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33
Q

Causes for AG metabolic acidosis

A

MUDPILES

  • Methanol, Metformin
  • Uremia
  • DKA, EtOH ketoacidosis, starvation ketoacidosis
  • Phenformin, Paraldehyde
  • Iron, isoniazid, inhalants (cyanide, carbon monoxide)
  • Lactic acidosis
  • Ethylene glycol
  • Salicylates
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34
Q

Compensation for acute respiratory acidosis

A

For every 10 increase in CO2, bicarb rises by 1

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35
Q

Compensation for metabolic alkalosis

A

For every 1 increase in bicarb, PCO2 increases by 0.7

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36
Q

Compensation for metabolic acidosis

A

For every 1 drop in bicarb, PCO2 drops by 1.2

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37
Q

Compensation for acute respiratory alkalosis

A

For every 10 decrease in CO2, bicarb decreases by 2

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38
Q

Compensation for chronic respiratory acidosis

A

For every 10 increase in CO2, bicarb rises by 4

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39
Q

Compensation for chronic respiratory alkalosis

A

For every 10 decrease in CO2, bicarb decreases by 4

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40
Q

Typical angina includes all 3 of

A
  1. Retrosternal chest pain
  2. Exacerbated by stress/emotion
  3. Relieved by nitro/rest
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41
Q

Atypical angina includes

A

2 of:

  1. Retrosternal chest pain
  2. Exacerbated by stress/emotion
  3. Relieved by nitro/rest
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42
Q

Non-cardiac chest pain includes

A

0-1 of:

  1. Retrosternal chest pain
  2. Exacerbated by stress/emotion
  3. Relieved by nitro/rest
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43
Q

Classes of angina

A

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

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44
Q

Unstable angina includes

A

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)
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45
Q

Trop repeat at

A

3-6h

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46
Q

STEMI tx

A 
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
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47
Q

STEMI dx

A

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

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48
Q

NSTEMI dx

A

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

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49
Q

TIMI

A

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

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50
Q

Long-term prevention for myocardial recovery

A 
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
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51
Q

Lateral leads represent

A

Left circumflex artery

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52
Q

Antero-septal leads represent

A

LAD artery

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53
Q

Inferior leads represent

A

Right coronary artery

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54
Q

Absolute C/I to thrombolysis (6)

A 
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
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55
Q

Relative C/I to thrombolysis (10)

A 
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
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56
Q

Aortic stenosis

A

Early-late peaking systolic murmur (crescendo-decrescendo)

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57
Q

Aortic regurgitation

A

Early diastolic or holo-diastolic murmur, blowing

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58
Q

Mitral stenosis

A

Low-pitched mid-diastolic rumble with opening snap

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59
Q

Medications for mitral stenosis

A

Negative chronaotropic agents and HR control (BB and CCB)

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60
Q

Mitral regurgitation

A

Holosystolic murmur over apex

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61
Q

EtOH Hepatitis

A 
AST:ALT = 2:1 
GGT elevated
IgA elevated 
Ferritin elevated
That N
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62
Q

AI hepatitis

A 
ASMA + 
ANA + 
ALKM + (in children)
Very high bill, ALT and AST 
High GGT, ALP 
IgG elevated
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63
Q

Wilson’s

A

Ap7B mutation
Low ceruloplasmin
High 24h urine copper

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64
Q

Wilson’s tx

A

Chelation with penicillamine

Maintenance with zinc

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65
Q

Hemochromatosis

A

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

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66
Q

Hemochromatosis tx

A

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

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67
Q

NAFLD

A

General transaminitis

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68
Q

NAFLD tx

A

Weight loss, fatty!

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69
Q

PBC

A 
Intra-hepatic only
Classic picture = young female 
Very increased bill, GGT, ALP
Increased ALT, AST 
Increased IgM 
AMA +
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70
Q

PBC tx

A 
Urodeoxycholic acid (UDCA)
Transplant
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71
Q

PSC

A 
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
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72
Q

PSC tx

A

ERCP for strictures

Transplant

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73
Q

Negative inotrope examples

A

BB
CCB
Class IA antiarrhythmic agents (procainamied)

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74
Q

Positive inotrope examples

A 
Digoxin
Amiodarone 
Calcium
Catecholamines - Dobutamine, epinephrine, norepinephrine 
PDEi - Milrinone
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75
Q

Orthostatic hypotension

A

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.

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76
Q

Protease affected in TTP

A

ADAMTS13

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77
Q

Classic pentad of TTP

A 
Thrombocytopenia
MAHA
Renal failure 
Fever
Mental status change
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78
Q

Main tx for TTP

A

PLEX (plasma exchange) - replace ADAMTS13

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79
Q

Classic triad HUS

A

MAHA
Thrombocytopenia
Acute renal failure

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80
Q

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

A 
Hx: Drugs, HIV, pregnancy, malignancy, diarrhea, AI disease 
Plts: Low 
Smear: Many schistos, large plts
Fibrinogen: Normal
INR/PTT: Normal
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81
Q

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

A 
Hx: sepsis, trauma. malignancy, obstetrical complications
Plts: Low
Smear: Fewer schistos, large plts
Fibrinogen: low 
INR/PTT: high
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82
Q

Thrombocytopenia

A

Plts <150 000/uL

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83
Q

HUS

A

Commonly a/w shiga-toxin producing E. coli

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84
Q

DIC

A

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

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85
Q

Only possible cause of single digit platelet levels

A

Immune thrombocytopenia

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86
Q

ITP first line tx

A

Steroids (prednisone) for ~4wks

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87
Q

ITP second line tx

A 
IVIG
Rituximab 
New TPO agonists 
Splenectomy 
Rhogam in Rh+ pts
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88
Q

Type I HIT (heparin-induced thrombocytopenia)

A

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

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89
Q

Type II HITT (heparin-induced thrombocytopenia with thrombosis)

A

Usually within 5-10d after exposure

ABs target heparin + PF4 complex –> immune complex that aggregates platelets = thrombocytopenia and thrombosis

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90
Q

HITT tx

A 
Stop heparin 
Alternate anticoagulant (danaparoid, bivalrudin, argatroban) until plts back to normal, then switch to warfarin with 5d overlap
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91
Q

PTH function

A
  1. Increases reabsorption of Ca2+ at distal tubule and bones
  2. Increases reabsorption of PO4 at proximal tubule
  3. Increases calcitriol
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92
Q

Drugs a/w hypercalcemia

A 
Vit D toxicity 
Thiazide 
Lithium
Tamoxifen
Tums
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93
Q

Symptoms of hypercalcemia

A

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

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94
Q

Tx of hypercalcemia

A
  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)
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95
Q

Role of calcitriol

A
  1. Increases Ca reabsorption in gut, kidney, and bone
  2. Increases PO4 reabsorption at gut, kidney
  3. Decreases PTH
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96
Q

Salbutamol

A

Ventolin

SABA

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97
Q

Ipratroprium bromide

A

Atrovent

SAMA

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98
Q

Lateral leads

A

I, aVL

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99
Q

inferior leads

A

II, III, aVF

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100
Q

Anteroseptal leads

A

V1, V2

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101
Q

Anterior leads

A

V3, V4

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102
Q

Anterolateral leads

A

V5, V6

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103
Q

NSTEMI ECG findings

A

ST-depression

T-wave inversion or flattening

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104
Q

Wellen’s sign

A

T-wave inversion or biphasic T-waves in V2-V4

Highly specific for critical stenosis of LAD

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105
Q

HFrEF

A

EF >40% –> systolic HF

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106
Q

HFpEF

A

EF > 40% –> diastolic HF

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107
Q

Systolic dysfunction

A

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

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108
Q

Diastolic dysfunction

A

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

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109
Q

NYHA classification of HF

A

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

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110
Q

Why CHFe now?

A 
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)
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111
Q

EHS in systolic heart failure

A

S3

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112
Q

EHS in diastolic heart failure

A

S4

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113
Q

BNP sensitivity vs specificity

A

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)

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114
Q

5 key CXR findings in CHF

A
  1. Increased cardio thoracic ratio (Cardiomegaly)
  2. Vascular redistribution
  3. Kerly-B lines
  4. Peri-bronchial cuffing
  5. Pleural effusions and/or pulmonary edema
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115
Q

BNP results

A 
<100 = unlikely HF 
100-250 = compensated LV dysfunction
250-500 = Diastolic and systolic dysfunction
500-1000 = Decompensated 
>1000 = severe HF
116
Q

CHF acute tx

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

NO BETA BLOCKERS

117
Q

CHF chronic tx (triple therapy)

A

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

118
Q

Non-drug therapies for HF

A
  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
Q

FEV1/FVC dx for COPD

120
Q

TLC dx for restrictive lung disease

121
Q

Ascites

A

(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
Q

SAAG

A

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

123
Q

Spironolactone : Lasix ratio

124
Q

Tx for acetaminophen overdose

A

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

125
Q

SBP features

A

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

126
Q

SBP microbiology

A

E. Coli > Klebsiella > Streptococcus pneumoniae

usually mono microbial, if poly microbial then consider GI perforation

127
Q

SBP tx

A

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

128
Q

Type I hepatorenal syndrome

A

Rapid onset, prognosis of 2-3 months

More serious

129
Q

Type II hepatorenal syndrome

A

Gradual onset, prognosis of 6-9 months

130
Q

Hepatorenal syndrome pathophysiology

A

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
Q

Hepatorenal syndrome dx

A 
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
Q

Hepatorenal syndrome tx

A

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

133
Q

Pancreatitis causes

A 
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
Q

Transudative causes of pleural effusion

A 
SYSTEMIC illness (low protein,  oncotic vs hydrostatic pressure imbalance) 
- HF, hypoalbuminemia (cirrhosis, malnutrition, nephrotic syndrome), SVC obstruction, atelectasis, trapped lung, peritoneal dialysis, PE
135
Q

Exudative causes of pleural effusion

A 
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
Q

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

A

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
Q

Microvascular complications of diabetes

A

Neuropathy
Nephropathy
Retinopathy

138
Q

Macovascular complications of diabetes

A

CVD
PAD
CAD

139
Q

Insulin titration for DKA

A

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
Q

Key features of HHS (Hyperosmolar hyperglycaemic state)

A

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

141
Q

Typical DKA patient

A

Young, T1DM

142
Q

Typical HHS patient

A

Older, T2DM

143
Q

Main form of tx for HHS patients

A

Fluids

Requires less insulin to close AG

144
Q

Rapid acting insulin

A

Humalog (Insulin lispro)

NovoRapid (Insulin aspart)

145
Q

Short acting insulin

A

Humulin-R

Novolin ge Toronto

146
Q

Intermediate acting

A

Humulin-N

Novolin ge NPH

147
Q

Long-acting basal insulin analogues

A 
Insulin detemir (Levemir)
Insulin glargine (Lantus)
148
Q

Pre-mixed insulin

A

Humulin
Novolin
Humalog
Novo Mix

149
Q

Drugs associated with SIADH

A 
SOMA 
S = SSRIs
O = Opioids
M = MDMA
A = Anti-convulsants
150
Q

Calculating serum osmolality

A

(2x Na) + Glucose + BUN

151
Q

SIADH causes

A

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

152
Q

Na+ correction in hyperglycaemia

A

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

153
Q

Cause of hyperosmolar hyponatremia

A

Hyperglycemia

154
Q

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

A

Urine osm > 500

Urine Na < 20 (Aldo NOT working)

155
Q

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

A

Urine osm >100

Urine Na <20 (Aldo IS working)

156
Q

Expected urine osm and urine Na in SIADH

A

Urine osm >100 (often >300)

Urine Na >40 (Aldo not affected b/c euvolemic state)

157
Q

Disease associated with rapid correction of hypovolemic hyponatremia

A

Osmotic demyelination syndrome

158
Q

Definition of hypernatremia

A

Serum Na+ > 145mmol/L

159
Q

Treatment for central diabetes insipidus

160
Q

Euvolemic causes of hypernatremia

A
  • 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
Q

Heparin antidote

162
Q

Octreotide

A

Somatostatin analogy - lowers portal venous pressure

163
Q

Labetolol

A

Alpha 1 and beta 1 and 2 blockers

164
Q

Nitroprusside

A

Use in hypertensive urgency/emergency

Affects arterial and venous dilation

165
Q

Hydralazine

A

Arteriolar dilator

166
Q

Secondary causes of HTN

A 
CNS
Hyperthyroid
OSA
Aortic coarctation 
Adrenals - pheo, cushings, hyperaldo
Renal
167
Q

Causes of renal artery stenosis

A

Atherosclerosis
Aneurysm
Fibromuscular dysplasia
Vasculitis

168
Q

When to switch to SC insulin

A

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

169
Q

Na+ correction in hyperglycaemia

A

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

170
Q

Pericarditis ECG findings

A

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

171
Q

Ischemia ECG findings

A

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

172
Q

RBBB ECG findings

A

Wide QRS in most leads

RSR’ in V1/V2

173
Q

LBBB ECG findings

A

Wide QRS in most leads

Notched R-wave in V5/V6

174
Q

Right-sided leads

175
Q

Left-sided leads

176
Q

1st degree AV block

A

Increased PR interval >200ms

PR interval constant

177
Q

2nd degree AV block, Mobitz Type I

A

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

178
Q

2nd degree AV block, Mobitz Type II

A 
Constant PR (either normal or prolonged) with random failures 
Associated with His-Bundle disease
179
Q

3rd degree AV block

A

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

180
Q

LVH ECG findings

A
  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
Q

RVH ECG findings

A
  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
Q

Causes of secondary hypertension

A

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
Q

Hyperaldosteronism workup

A

Serum renin/aldosterone

Hypokalemia

184
Q

Pheochromocytoma workup

A

24h urine metanephrines

185
Q

Cushing’s workup

A

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

186
Q

Renovascular workup

A

Renal doppler US
CT/MRI angiogram
Renal angiogram

187
Q

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

A

Beta blocker

188
Q

Medications with proven mortality benefit for hypertension

A

ACEi and Chlorthalidone (diuretic)

189
Q

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

A

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

190
Q

HTN drug combos to avoid

A

ACEi and ARB

Diltiazem and Metoprolol (Non-DHP CCB and BB)

191
Q

First line agents for HTN in pt with stable angina

A

BB
Long-acting CCB
ACEi

192
Q

First line agents for HTN in pt with recent ACS

A

BB

ACEi/ARB

193
Q

First line agents for HTN in pt with decreased LVEF

A

ACEi/ARB
BB
Nitro/hydralazine
Aldosterone antagonists

194
Q

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

A

ACEi/ARB
Thiazide
Loop for volume control

195
Q

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

A

ACEi/ARB or thiazide or ND-CCB

196
Q

First line agents for HTN in pt with diabetes with nephropathy

A

ACEi/ARB then ND-CCB

197
Q

CCB dyhydropyridine

A

Potent vasodilators

Ex. Nifedipine, amlodipine, felodipine

198
Q

CCB non-dihydropyridine

A

HR control

Ex. Verapamil, diltiazem

199
Q

S/E of thiazides

A

Hypokalemia, hyponatremia, worsening gout

200
Q

S/E of ACEi/ARBs

A

Hyperkalemia, renal failure

201
Q

S/E of CCB DHP

A

Peripheral edema

202
Q

S/E of CCB non-DHP

A

Bradycardia, confusion

203
Q

S/E of BB

A

Fatigue, ED, bradycardia, depression

204
Q

Hypertensive emergency

A

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
Q

Hypertensive urgency

A

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
Q

Late systolic murmur

A

Mitral valve prolapse

207
Q

Aortic valve murmur radiation

208
Q

Pulmonic valve murmur radiation

A

Left shoulder

209
Q

Tricuspid valve murmur radiation

A

xiphoid right of sternum

210
Q

Mitral valve murmur radiation

211
Q

AKI

A

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

212
Q

Causes of nephritic syndrome

A 
Anti-GBM (Good Pasture's) 
IgA Nephropathy 
Membranoproliferative glomerulonephritis
Secondary to SLE, HBV, HCV
Pauci-immune
213
Q

Nephrotic syndrome proteinuria

214
Q

Causes of nephrotic syndrome

A 
Focal segmental glomerulosclerosis 
Membranous nephropathy 
Minimal change disease
Membranoproliferative GN 
Secondary to DM, obesity, AI, Infectious, drugs (NSAIDs, lithium, heroin), malignancy
215
Q

Clinical feature of nephrotic syndrome

A 
PALE 
Proteinuria (>3.5g/d) 
hypoAlbuminemia 
hyperLipidemia 
Edema 
\+ hyper coagulable state (lose protein C&amp;S and antithrombin), immunosuppression (lose immunoglobulins) 
GFR usually preserved
216
Q

2 causes of ATN

A

Ischemic (pre-renal causing renal)

Toxic (drugs - acyclovir, ahminoglycosides, contrast, pigment, myoglobin, protein)

217
Q

Casts seen in pre-renal causes

218
Q

Casts seen in nephritic syndrome

219
Q

Casts seen in nephrotic syndrome

A

Fatty casts/oval bodies

220
Q

Casts seen in ATN

A

Muddy brown casts

221
Q

Causes of acute interstitial nephritis

A

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

222
Q

Trio of AIN

A

Fever
Rash
Eosinophilia
+/- urine eosinophils and WBC casts

223
Q

Vascular causes of renal AKI

A

MAHA
Embolic
Vasculitis

224
Q

Functional excretion of Na+

A

(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
Q

AIN or pyelonephritis casts

226
Q

Urine osmolality based on pre-renal vs renal

A

Pre-renal: Uosm >500

Renal: Uosm 250-300

227
Q

SLE special tests to order

A

C3, C4, ANA, anti-dsDNA

228
Q

Post-infectious causes of AKI special tests to order

A

Anti-streptolysin O Titre

229
Q

IE special test to order

A

Blood cultures

230
Q

Membranoprolifer glomerulonephritis special tests to order

A

HBV, HCV, HIV

231
Q

Anti-GBM disease special tests to order

A

Anti-GBM antibody

232
Q

Pauci-immune

A

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
Q

Pauci-immune special test to order

234
Q

Multiple myeloma special test to order

235
Q

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

A 
Hyaline casts
20:1 
<1% 
>500mOsm
<20
236
Q

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

A 
Abnormal casts (RBC, fatty, muddy brown/heme granular) 
<20:1 
>1% 
250-300mOsm 
>40
237
Q

Indications for dialysis

A

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
Q

Azotemia

A

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

239
Q

Minimal change disease

A

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

240
Q

Membranous glomerulonephropathy (MGN)

A

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
Q

Membranoproliferative glomerulonephritis

A

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
Q

Focal segmental glomerulosclerosis

A

More severe form of MCD

Pure nephrotic

243
Q

Anti-GBM nephritis

A

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
Q

IgA nephropathy

A

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
Q

Alpha-1 receptors

A

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

246
Q

Beta-1 receptors

A

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

247
Q

1st line tx for anaphylactic shock

A

Epinephrine

248
Q

1st line tx for cardiogenic shock WITH pulmonary hypertension

A

Phosphodiesterase inhibitor (Milrinone)

249
Q

qSOFA

A

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

250
Q

SIRS

A 
>/2 of:
Temp >38.3C or <36C 
HR > 90BPM 
RR > 20
PaCO2 <32mmHg 
WBC >12 or <4
251
Q

Sepsis

A

SIRS + infection

252
Q

Anemia

A

<135g/L in men

<120g/L in women

253
Q

Microcytic anemia ddx

A 
MCV <80uL
TAILS 
Thalassemia 
Anemia of chronic disease
Iron deficiency anemia 
Lead poisoning 
Sideroblastic anemia
254
Q

Iron deficiency anemia

A

Low iron
Low ferritin
High transferrin (TIBC)
Low TSAT

255
Q

Increasing iron absorption

A

Vitamin C

Meat/fish

256
Q

Thalassemia dx

A 
Target cells on smear 
Narrow RDW, smaller MCV than Fe deficiency 
Less profound anemia 
Normal iron studies 
Hb electrophoresis
257
Q

Anemia of chronic disease

A
  • 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
Q

Retic count

A

Normal = 1%

Appropriately compensated anemia = 3-10%

259
Q

Tx for iron def anemia

A

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
Q

Anemia of chronic dz dx

A 
Normal or high ferritin 
Low Fe 
Low TIBC (diff from Fe-def)
Normal or low TSat 
Low relic
261
Q

Anemia of chronic dz tx

A

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

262
Q

Lead poisoning blood smear

A

Microcytic hypo chromic anemia with basophilic stippling

263
Q

Sideroblastic anemia

A

Impaired heme biosynthesis and increased cellular Fe uptake

Increased TSat
Decreased transferrin
Increased ferritin
Fe overload!

264
Q

Acquired causes of sideroblastic anemia

A 
EtOH 
Drugs (isoniazid, chloramphenicol, linezolid, Copper deficiency, zinc toxicity, hypothermia)
265
Q

Normocytic anemia

A

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

266
Q

AI hemolytic anemia

A

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

267
Q

Non-immune causes of hemolytic anemia

A

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

268
Q

G6PD deficiency

A

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

269
Q

Pyruvate kinase deficiency

A

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

270
Q

Normal BM but low retic normocytic anemia

A 
TACE 
Toxins 
Anemia of chronic disease
CKD 
Early Fe deficiency
271
Q

Abnormal BM and low retic normocytic anemia

A 
BM failure (aplastic anemia)
Infiltration (Heme - myeloma, indolent lymphoma, myelofibrosis, MDS; non-heme - solid tumour, infection, inflammatory)
272
Q

Microcytic anemia

A

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
Q

Warm agglutinins tx

A

Treat underlying disease
Steroids
Consider splenectomy or immunosuppressants
Transfuse with caution

274
Q

Cold agglutinins tx

A

Avoid cold

275
Q

Hemolytic anemia b/w

A 
Bili high
LDH high 
Haptoglobin low
Retics high
Smear - spherocytes (AI), schistocytes (MAHA)
276
Q

High protein states peripheral smear (ie.multiple myeloma)

277
Q

Cold agglutination peripheral smear

A

Agglutination

278
Q

Warm agglutinins peripheral smear

A

Spherocytes

279
Q

G6PD deficiency peripheral smear

A

Bite cells

280
Q

Thalssemia peripheral smear

A

Target cells

281
Q

Iron deficiency peripheral smear

A

Pencil cells

282
Q

Uremia peripheral smear

A

Burr cells

283
Q

MDS, megaloblastic peripheral smear

A

howell jolly body

284
Q

ECG of hyperkalemia

A

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

285
Q

AKI dx criteria

A

Increase in serum Cr by >/= 26umol/L within 48h or by >/= 50-100% from baseline
Urine output <0.5ml/kg/h for 6h
NOT based on GFR

Clerkship (7 decks)

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