Internal Flashcards
1
Q
Symptoms of hyponatremia
A
Usually related to water shifts from brain (cerebral edema) –> lethargy, confusion, coma, seizures
2
Q
Hyponatremia values
A
<135mmol/L
3
Q
H. Pylori infection treatment
A
PPI (lansoprazole) + 2 antibiotics (usually clarithromycin + amoxicillin) for 14days
4
Q
Common causes of hypervolemia
A
Congestive heart failure
Cirrhosis
Nephrotic syndrome
5
Q
Common treatment for hyponatremia
A
Diuretics
6
Q
Most common cause of euvolemic hyponatremia
A
Syndrome of inappropriate ADH
7
Q
Aortic dissection
A
Tear in intima to allow false lumen through media
8
Q
ABG
Ph/pco2/po2/hco3
A
7.4/40/100/24
9
Q
Causes of low albumin
A
Liver disease (ie cirrhosis)
Renal disease
Malnutrition
10
Q
NT associated with Parkinson’s
A
Dopamine
11
Q
COPD
A
Progressive airflow limitation associated with abnormal inflammatory response to noxious stimulants
12
Q
2 main branches of COPD
A
Chronic bronchitis
Emphysema
13
Q
Symptoms of ICP
A
Headache
Nausea
Vomiting
Papilledema
14
Q
Advil
A
Ibuprofen
15
Q
Tylenol
A
Acetaminophen
16
Q
Aspirin
A
Acetylsalicylic acid
17
Q
Possible causes of pulmonary embolism
A
Endothelial injury (ie. surgery)
Stasis (ie. pregnancy)
Hypercoagulation
18
Q
Diastolic murmurs
A
Aortic regurgitation
Mitral stenosis
19
Q
Systolic murmurs
A
Mitral regurgitation
Aortic stenosis
20
Q
COPD patient
A
Blue bloater
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)
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
23
Q
Negative inotropes
A
Weaken heart contraction
24
Q
Positive inotropes
A
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 (
285
AKI dx criteria
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
