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1
Q

Hallmark clinical manifestations of hyperkalemia:

A

Cardiac toxicity and peaked T waves, Ascending weakness

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2
Q

What factors are used to calculate the TIMI score for ACS?

A 
A - age (>65. >75)
M - markers positive (troponin, CK-MB)
E - ekg w/ st deviation
R - risk factors for CAD (>=3)
I - ischemia
C - known CAD
A - aspirin use in last 7 days
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3
Q

After identifying that a patient has nephritic syndrome, what is the next test to order to narrow the ddx?

A

Serum complement

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4
Q

What medical management might you use in a patient you believe to have a true total body excess of potassium (v. hyperkalemia)?

A

Kayexalate (ion exchange resin)
Diuretic
Dialysis

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5
Q

When is thrombolysis indicated in the setting of a PE?

A

Hemodynamically unstable (i.e. shock, RHF)

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6
Q

Hallmark clinical manifestations of hypokalemia:

A

Weakness or paralysis
Ileus
EKG changes: flattened T waves, prominent U waves

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7
Q

Plasma osmolality is determined primarily by (3):

A
  1. Sodium
  2. Glucose
  3. BUN
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8
Q

Medical DVT prophylaxis of choice in a patient with CKD.

A

Heparin (no renal clearance)

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9
Q

3 features of Alport’s syndrome:

A
  1. isolated hematuria
  2. sensorineural deafness
  3. ocular problems (i.e.lens dislocation, cataracts…)
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10
Q

EKG shows ST elevation in the inferior lead and V1-V3, what artery was most likely occluded?

A

R coronary artery.

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11
Q

First line antibiotic regimen for CAP.

A

Macrolide (azithromycin, clarithromycin)

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12
Q

Standard medical therapy for all ACS:

A
  1. Aspirin or clopidogrel (anti-platelet)
  2. Bblocker
  3. Nitroglycerin
  4. Morphine
  5. Oxygen
  6. LMWH or heparin (anti-coag)
  7. ACEI or ARB (remodeling)
  8. GP IIb/IIIa inhibitors - if PCI
  9. STATIN
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13
Q

CURB-65 Guidelines for risk stratification in CAP.

A 
Confusion
Uremia (BUN >20)
Respirations > 30
Blood Pressure 
Age >65
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14
Q

Coverage for Pneumocystis

A

Bactrim

TMP-SMX

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15
Q

Heparin-Induced Thrombocytopenia (HIT)

A

A thrombocytopenia with >50% decrease in platelets occurring 5-10 days after administration of heparin.

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16
Q

Systems to consider in DDx of chest pain (5).

A 
Cardio
Pulm
GI
MSK
Psych (anxiety)
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17
Q

A patient with a history of asthma is being evaluated for nephritic syndrome. What is likely to be seen on renal biopsy?

A

Granulomatous inflammation, eosinophilia

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18
Q

How might an MI cause hypokalemia?

A

Catecholamine excess! Drives potassium into intracellular space.

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19
Q

EKG shows ST elevation in leads V5-V6, I, II, and aVL. What artery was most likely occluded?

A

L circumflex artery.

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20
Q

What are the 3 broad categories of ATN etiologies?

A
  1. Ischemia (progression of pre-renal AKI)
  2. Contrast
  3. Toxins
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21
Q

How does Goodpasture syndrome differ from Wegener’s granulomatosis in presentation?

A

Renal and pulmonary involvement in both.

Wegener’s with involvement of upper respiratory tract as well (epistaxis, perforation of septum…)

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22
Q

Nephrotic syndrome is characterized by heavy proteinuria and what other hallmarks?

A 
Hypoalbuminemia 
Edema
Hypercoagulability
Hypogammaglobulinemia
Hyperlipidemia
Lipiduria
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23
Q

Membranous nephropathy associated diseases:

A

Hep B/C, tumors, SLE

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24
Q

Physical examination findings in heart failure:

A

JVD, crackles, S3, hypotension, cool extremities

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25
Q

What tests might you order if a patient with pneumonia fails to respond within 72 hours?

A

Drug levels
Bronchoscopy (resistant organisms?)
Chest CT (fungal/viral v. complication)

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26
Q

What are the drugs known to cause ATN?

A

Aminoglycosides (i.e. gentamycin), vancomycin, amphotericin, cisplatin

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27
Q

Most important factors in predicting all-cause mortality after STEMI:

A

Age (>65, esp >75)
Systolic BP > 100
HR

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28
Q

Antibiotic regimen for HAP.

A

MRSA: vancomycin
Pseudomonas: pip/tazo, cefepime, or carbapenem
Others: FQ or [gentamicin + azithromycin]

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29
Q

What medications can be used for hyperkalemic patients in order to cause K+ shift back into cells?

A

Glucose + insulin
Bicarbonate (H+ out, K+ in)
Beta agonist i.e. albuterol (catecholamines)

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30
Q

What are some drugs that can cause pre-renal azotemia?

A

NSAIDs, Cyclosporine: vasoconstriction of afferent arteriole (block PGs)

ACEi, ARB: vasodilation of efferent arteriole (block angiotensin II)
CONTRAST

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31
Q

When is a chest tube indicated in a patient with pneumonia?

A

Loculated effusion
Pleural fluid with positive gram stain or culture.
pH 3x ULN

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32
Q

What urine sediment findings are indicative of ATN?

A

Muddy brown granular casts, tubular casts

+/- RBC, protein

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33
Q

What urine sediment findings are indicative of GN?

A

RBC casts with dysmorphic RBCs

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34
Q

How is hyperkalemia treated urgently (i.e. serum K > 6, patient with EKG changes)?

A

Calcium gluconate

also monitor EKG

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35
Q

Stimuli for ADH release:

A 
High serum osmolality
Low blood volume
Angiotensin-II
Pain
Nausea (powerful)
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36
Q

How is post-renal azotemia diagnosed?

A

Catheterization with >100 mL remaining in bladder after voiding.

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37
Q

Modified Well’s criteria for PE:

A 
DVT sx.
PE is most likely
Tachycardia
Immobilization/Surgery
Hx of DVT or PE
Hemoptysis
Cancer in last 6 mo.
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38
Q

How to differentiate UA from NSTEMI.

A

Biomarkers. In NSTEMI there is release of troponins or CK-MB.

Also, NSTEMI does not respond to nitroglycerin.

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39
Q

Most common organisms causing catheter-associated UTI:

A

Yeast, E. coli

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40
Q

Virchow’s triad

A
  1. Endothelial injury
  2. Venous stasis
  3. Hypercoagulability
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41
Q

Most common causes of AKI in the ICU (4)

A

Sepsis
Major surgery
Low CO/hypovolemia
Drugs

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42
Q

A patient with nephritic syndrome is found to have low serum complement. What is your differential diagnosis?

A

Post-streptococcal GN

Lupus nephritis
Membranoproliferative GN
Infective endocarditis

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43
Q

Long term complications/sequelae after a PE:

A

Pulmonary hypertension

Arrhythmias

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44
Q

What other electrolyte should always be checked in a hypokalemic patient and why?

A

Magnesium

It blocks potassium excretion in the tubules, need to correct both to correct K.

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45
Q

Where in the kidneys is K+ actively excreted?

A

The distal tubule (by principle cells)

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46
Q

When should the FE of urea be used over the FE of sodium and why?

A

When a patient has taken a diuretic because FE of sodium will be high regardless of renal function.

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47
Q

Well’s Criteria for DVT:

A 
Cancer w/i 6 mo.
Immobilization
Bedridden/surgery
Tenderness along deep vein distribution
Swelling of entire leg
Swelling of calf
Unilateral pitting edema
Collateral superficial veins
Previous DVT
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48
Q

A patient with nephritic syndrome is found to have a normal serum complement. What is your differential diagnosis and what tests will you use to differentiate?

A

Goodpasture syndrome/anti-GBM disease: test for anti-GBM antibodies
Wegener’s Granulomatosis: test for ANCA, will be C-ANCA positive
Microscopic polyangitis: P-ANCA positive
Churg-Strauss syndrome: P-ANCA positive

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49
Q

Light’s Criteria:

Exudate If….

A

Pleural fluid protein/serum protein > 0.5
Pleural fluid LDH/serum LDH > 0.6
Pleural fluid LDH > 2/3 ULN

(Otherwise, transudate)

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50
Q

How is HIT treated?

A

Stop the heparin.
Give direct thrombin inhibitors (lepirudin, argatroban, danaparoid) as alternative anticoagulation and bridge to warfarin when platelet count is >150k.

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51
Q

What are endogenous toxins that may cause ATN?

A

Hemoglobin, myoglobin

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52
Q

What urine sediment findings are indicative of AIN?

A

WBC casts, WBC with negative urine culture

+/- RBCs

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53
Q

Nephritic syndrome is characterized by hematuria and what other hallmarks?

A

Mild proteinuria
Azotemia/oliguria
Salt retention w/ periorbital edema and HTN
Dysmorphic RBCs in urine

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54
Q

Most common organisms isolated in surgical site infections.

A

S. aureus and other staphylococcus, Enterococcus, Pseudomonas

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55
Q

For external balance of potassium, what are 3 factors controlling K+ excretion?

A
  1. Na+ delivery to the distal tubule (increased distal tubular flow = increased K+ excretion)
  2. Acid/Base status (decreased H+ excretion = increased K+ excretion)
  3. Aldosterone (induces transcription/placement of Na channels and Na-K pump in principle cells)
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56
Q

Most common organism causing bacteremia associated with lines.

A

S. epidermis

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57
Q

When is a CXR indicated for evaluation of a cough?

A

If accompanied by 1 or more:

Fever > 100
Tachycardia
2: rales, decreased breath sounds, no asthma history
Not improving or worsening

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58
Q

DDX Nephrotic syndrome (5):

A 
Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy
Diabetic nephropathy
Systemic amyloidosis
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59
Q

A 23 year old male comes to the doctor because he recently noticed blood in his urine. He had a cold this week, but is otherwise healthy. What is the most likely diagnosis?

A

IgA Nephropathy

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60
Q

When is a TEE indicated in a patient with bacteremia?

A

If organism isolated is S. aureus.

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61
Q

Antibiotics associated with C. diff colitis

A

Clindamycin
Ampicillin
Cephalosporins
Fluoroquinolones

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62
Q

DDx for hyperosmolality:

A

Hypernatremia
Hyperglycemia
Renal failure (high BUN)

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63
Q

What is a normal range for plasma osmolality?

A

275-290 mOsm/kg

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64
Q

A patient identified to have a nephritic syndrome also has wrist drop and foot drop. What is the most likely diagnosis?

A

Microscopic polyangitis

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65
Q

Etiology of Alport’s syndrome.

A

Defect of type IV collagen.

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66
Q

CAP antibiotics if admitted as an inpatient.

A

Macrolide + 3rd gen cephalosporin (cefotaxime, ceftriaxone)
OR
Fluoroquinolone

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67
Q

Medical DVT prophylaxis of choice in a cancer patient?

A

Lovenox (enoxaparin)

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68
Q

EKG shows ST elevation in leads V1-V5, most prominent in V2 and V3. There is also ST elevation in lead I and aVL with mild ST depression in aVR. What artery was likely occluded?

A

Left anterior descending.

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69
Q

When is a thoracentesis indicated?

A

New pleural effusion > 1cm on lateral decubitus.

Parapneumonic effusion.

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70
Q

What antibiotics can be used to treat MRSA?

A

Vancomycin
Linezolid
Daptomycin

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71
Q

How does acidosis affect serum potassium?

A

Hyperkalemia

shift of H+ into cell (in an attempt to reduce acidosis) causes shift of K+ out of cell (and into serum).

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72
Q

What drugs are known to cause an allergic interstitial nephritis?

A

B-lactams and other sulfa drugs, NSAIDs, PPIs

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73
Q

Antibiotics used to treat C. diff colitis.

A

Metronidazole

Vancomycin

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74
Q

How does severe hyperglycemia affect serum potassium?

A

Hyperkalemia

Hypertonic serum creates a solvent drag, this pulls water out of the cells and K+ follows.

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75
Q

Indications for dialysis: (AEIOU)

A

AEIOU refractory to therapy:

Acidemia
Electrolyte disturbances (hyperkalemia, hyperphosphatemia, tumor lysis)
Intoxication
Overload of fluid
Uremia w/ symptoms (esp. with pericarditis)

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76
Q

How to monitor heparin anticoagulation?

A

PTT, platelet count

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77
Q

What are the different hepatocellular injury processes in liver disease?

A

Hemochromatosis
Wilson’s disease
Alcoholic hepatitis
Hepatitis A, B, C

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78
Q

What are the different cholestatic injury processes in liver disease?

A

NASH
Primary Biliary Sclerosis
Primary Biliary Cirrhosis

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79
Q

What are the laboratory findings in alcoholic hepatitis?

A

AST > ALT (>2:1) but not severe electation
Increased MCV of RBCs
Increased GGT

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80
Q

What will be shown in a liver biopsy of alcoholic hepatitis?

A

hepatocyte necrosis, Mallory bodies

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81
Q

How soon after exposure to hepatitis would you see…

IgM
HbsAg
HCV RNA

A

Igm HepA - early

HbsAg - early

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82
Q

SAAG =

A

Serum ascites-albumin gradient =

serum albumin - ascitic fluid albumin

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83
Q

SAAG greater than 1.1 –>

A

Transudate –> portal hypertension

Causes: Cirrhosis, SBP, acute hepatitis, RHF, venous thrombosis, Schisto

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84
Q

SAAG less than 1.1 –>

A

Exudate

Causes: Peritoneal carcinomatosis, pancreatitis, peritoneal dialysis

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85
Q

How do you diagnose Spontaneous Bacterial Peritonitis?

A

Greater than 250 PMN – Blood cx at bedside increases yield of + cultures in SBP

Treatment:

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86
Q

How do you evaluate hepatic encephalopathy?

A

NH3 does not correlate well

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87
Q

How do you treat uncomplicated DVT?

A

Bridging heparin –> warfarin

Shorter warfarin course if provoked

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88
Q

How do you distinguish pre-renal from intra- or post-renal causes of AKI?

A

Fractional Excretion of Sodium or Urea

– Tubules will be intact in pre-renal cause, FENa

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89
Q

How do you treat a severe GI bleed?

A

2 large bore IVs
cross and type
aggressive in IVF resuscitation

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90
Q

Delirium is commonly caused by…

A

Drugs, Electrolytes, Lack of drugs, Infection, Reduced sensory input, Ictal, Urinary/Fecal retention, Metabolic, Stroke/Subdural

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91
Q

How do you treat uncomplicated DVT?

A

Bridging heparin –> warfarin

Shorter warfarin course if provoked

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92
Q

How do you treat STEMI?

A

Agressive Thrombolysis

i. PCI w/in 90 min or to PCI hosp w/in 2 hours
ii. thrombolysis w/in 30 min

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93
Q

What are the early complications of MI?

A

V-fib, new murmurs

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94
Q

What are the late complications of MI?

A

pericarditis, aneurysms, CHF

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95
Q

What is the treatment bundle for VAP?

A

limit prolonged ventiliation, increase stomach pH (no antacids), elevate head of bed 30-45, chlorhexadine rinse

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96
Q

If pH is normal,
CO2 is high,
bicarb is high
then you have…

A

Respiratory acidosis and metabolic alkalosis

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97
Q

What can lead to pseudohyperkalemia?

A

high cell counts, hemolyzed, traumatic blood draws

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98
Q

If AG is high and pH, CO2 and bicarb are normal then you have…

A

AG metabolic acidosis + metabolic alkalosis

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99
Q

If AG, pH, CO2 and bicarb are ALL normal then you have…

A

Non-AG metabolic acidosis + metabolic alkalosis OR Normal

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100
Q

If pH and bicarb are low …

A

It’s metabolic acidosis

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Perfectly
101
Q

What are the steps to evaluating Acid-Base disorders?

A

1) Classify primary disturbance (Acidosis/Alkalosis, Metabolic/Respiratory)
2) Determine compensation
3) Calculate Anion Gap (AG = Na-[Cl+HCO3])
4) Calculate potential bicarb (= HCO3 + ChangeAG)

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102
Q

If pH and bicarb are high…

A

Metabolic alkalosis

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103
Q

How does low albumin affect the anion gap?

A

Low albumin lowers the expected anion gap

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104
Q

How do you determine if there is respiratory compensation in metabolic acidosis?

A

WINTER’s FORMULA
Expected pCO2 = [1.5(HCO3) + 8] +/-2

If pCO2 is HIGHER than expected –> resp acidosis

If pCO2 is LOWER than expected –> resp alkalosis

105
Q

How does RTA change the urine anion gap?

A

Usually UAG = UNa + UK - UCl

A positive urine anion gap suggests a low urinary NH4+ (as in RTA).

NH4+ is the most important unmeasured ion in urine (accompanied by the anion chloride).

A negative urine anion gap can be used as evidence of increased NH4+ excretion. (diarrhea)

106
Q

What factors must be reviewed on X-ray to evaluate it’s accuracy?

A

Degree of rotation
Level of penetration
Amount of exposure
Level of inspiration

107
Q

What is the finding to look for on a lateral chest x-ray film?

A

Spine sign

108
Q

How do you determine if there is respiratory compensation in metabolic alkalosis?

A

Expected pCO2 = 0.8(changeHCO3) + 40

If pCO2 HIGHER than expected –> resp acidosis

If pCO2 LOWER than expected –> resp alkalosis

109
Q

What is the best test to diagnose PE?

A

Spiral CT

V/Q scan

110
Q

What are the components of Virchow’s Triad?

A

endothelial injury, venous stasis, hypercoagulable state

111
Q

What are the main risk factors for DVT?

A

immobilization, cancer (tissue factor), surgery

smoking, prior DVT/PE, OCPs, pregnancy, nephrotic syndrome, heart failure, liver failure, antiphospholipid, HIT, tamoxifen, raloxifene, indwelling venous catheter, chemotherapy, growth factors, obesity

112
Q

What are hereditary risk factors for DVT?

A

Factor V Leiden mutation, Protein C/S deficiency, prothrombin mutation, antithrombin deficiency, hyperhomocysteinemia

113
Q

What are the high risk DVT locations? (risk of embolization)

A

deep femoral veins, pelvic veins

114
Q

What drug can be used for DVT prophylaxis in CKD patients?

A

heparin (other drugs have renal clearance)

115
Q

What are the contraindications to anticoagulation?

A

high bleeding risk, liver disease, severe HTN, prior surgery/trauma, pregnancy (warfarin)

116
Q

What is the antidote to heparin and LMWH?

A

protamine

117
Q

Symptoms:

Dyspnea, pleuritic chest pain, cough, +/- hemoptysis –>

A

pulmonary embolus

118
Q

What will be the ABG findings of patients with PE?

A

low PaO2, low PaCO2, high pH

–> Respiratory alkalosis

119
Q

What lab test should be ordered to assess for LOW risk of DVT or PE?

A

D-dimer

120
Q

If you have a positive D-dimer, what test should follow for suspected DVT or PE?

A

DVT –> Ultrasound

PE –> Spiral CT/CTA (or V/Q scan if contrast allergy/CKD)

121
Q

How do you treat new DVT or hemodynamically stable PE?

A

Heparin/Lovenox anticoagulation –> Warfarin

If patient cannot tolerate anticoag –> IVC filter

Monitor heparin with PTT, platelets, warfarin with INR

Cancer: Lovenox + long term Lovenox

122
Q

What complications can arise from DVT?

A 
Post-thrombotic syndrome (venous insufficiency)
Compartment syndrome (blocked drainage)
123
Q

What are the typical organisms found in wound infections?

A

Surgical site: Staph. aureus, other staph

HA-bloodstream: Other staph, enterococcus, candida

124
Q

What are the typical organisms found in healthcare associated pneumonia?

A

Staph aureus/MRSA

GNRs: Pseudomonas, Klebsiella, E.coli, Enterobacter, Acinetobacter, Serratia

125
Q

What are the typical organisms found in healthcare associated UTIs?

A

E.coli

Catheter-associated: yeast, E.coli, CNR, enterococci, staph epi

126
Q

How do you treat UTI?

A

Uncomplicated: nitrofurantoin, TMP-SMX, FQ
Complicated: TMP-SMX, FQ (Cipro/Levo)

127
Q

What antibiotics might cause C.diff colitis?

A

Broad spectrum: clindamycin, ampicillin, cephalosporins, fluoroquinolones

128
Q

What antibiotics might treat C.diff colitis?

A

Metronidazole (1st line, mild-mod)
Vancomycin (severe based on WBC, Cr, age)

Use both if complications like ileus, megacolon, shock, peritonitis

129
Q

What can be used to treat MRSA?

A

vancomycin, daptomycin (not PNA), linezolid

130
Q

What can be used to treat VRE?

A

Daptomycin, linezolid

131
Q

What are the typical organisms found in Community Acquired Pneumonia?

A

Overall: Strep pneumo
COPD: H.influenzae, Moraxella
Young: Mycoplasma, Chlamydia, young
Elderly: Legionella

132
Q

How do you treat community acquired pneumonia?

A

1st line: macrolide
Doxycycline
Recent abx: Fluoroquinolone (levo, moxi)
Inpatient: macrolide + 3rd gen ceph or fluoroquinolone

133
Q

How do you diagnose C.diff colitis?

A

Stool EIA (toxins) or PCR or glutamate dehydrogenase

Only if the patient has symptoms, esp DIARRHEA

134
Q

How can C.diff colitis be treated?

A

Antibiotics (metronidazole -> vancomycin)
Stool transplant
CT + surgery if toxic megacolon
Probiotics

135
Q

How will hyperkalemia impact the EKG findings?

A

peaked T waves –> PR prolongation –> P-wave flattening –> QT prolongation –> sine waves

136
Q

How will hypokalemia impact the EKG findings?

A

U waves

137
Q

How will hypocalcemia impact the EKG findings?

A

QT prolongation (less Ca for action potential)

138
Q

How will hypercalcemia impact the EKG findings?

A

QT shortening (more Ca for action potential –> quicker)

139
Q

What are the criteria for AKI?

A

Creatinine increased by >/= 50% OR 0.3

OR Urine output decreased to

140
Q

What will the ABG show in renal failure?

A

Metabolic acidosis

141
Q

When should FENa be measured?

A

It shouldn’t, it will always be high

142
Q

When should FEUrea be measured?

A

If the patient has taken a diuretic

143
Q

What are possible causes of post-renal azotemia (high BUN)?

How to diagnose?

How to treat?

What are the sediment findings?

A

Outflow obstruction: BPH, prostate cancer, urethral stricture, bilateral compression (cancer, stones)

Diagnose with catheterization, renal ultrasound

Treat: catheterization, stents, underlying cause

Sediment findings: normal RBCs, no casts

144
Q

How does the length of time of pre-renal obstruction affect FENa?

A

Early: tubules intact, FENa 2%

145
Q

What can cause pre-renal azotemia?

What are the sediment findings?

A

Decreased blood flow: volume depletion, low CO, cirrhosis, sepsis, NSAIDs, cyclosporine, ACEIs, ARBs, orthostatic hypertension

Sediment findings: Bland, hyaline casts

146
Q

What does Angiotensin-II vasoconstrict?

A

Efferent Arteriole

147
Q

What drugs vasodilate the efferent arteriole?

A

ACEIs, ARBs (block Ang-II)

148
Q

What vasodilates the afferent arteriole?

A

Prostaglandins (released by sympathetic NS)

149
Q

What drugs vasoconstrict the afferent arteriole?

A

NSAIDs, cyclosporine (block PGs)

150
Q

What is the most common cause of altered mental status/delirium?

A

Hypoglycemia

151
Q

What are the risk factors for delirium?

A

elderly, polypharmacy, dementia, cognitive impairment, psychiatric condition, chronic medical
conditions, visual/hearing impairments, hospitalization, social isolation

152
Q

The onset is rapid, fluctuating, may included visual hallucinations or abnormal vital signs, and has altered consciousness

A

Delirium

153
Q

The onset is slow, progressive, and has degenerative changes

A

Dementia

154
Q

Causes of delirium include:

A 
Drugs
Electrolytes
Lack of Drugs
Infection
Reduced sensory
Ictal
Urinary/fecal retention
Metabolic
Stroke/subdural
155
Q

When would a lumbar puncture be indicated to evaluate for altered mental status?

A

Suspect meningitis, subarachnoid hemorrhage, autoimmune inflammation

156
Q

What three components make up the Glasgow Coma Scoring system?

A 
Eye opening (4-spontaneous to 1-none)
Verbal response (5-oriented to 1-none)
Motor response (6-obeys commands to 1-none)
157
Q

What medications can be used for delirium?

A

Thiamine –> glucose/dextrose
Haloperidol for agitation (monitor QTc)

AVOID benzos unless withdrawing

158
Q

Alcohol withdrawal symptoms begin when and include what?

A

6-48 hours after last drink

anxiety, agitation, tremor, HA, confusion, N/V, sweats, hallucinations x3 (visual, auditory, tactile)

159
Q

What are severe complications of withdrawal?

A

Seizures

160
Q

How do you treat alcohol withdrawal?

A

Benzodiazepines, thiamine –> glucose, replete K, Mg, PO4

161
Q

What might cause hepatic encephalopathy?

A

GI bleed, infection, constipation, hypoxia, electrolyte imbalance, sedatives/tranquilizers

162
Q

How do you treat hepatic encephalopathy?

A

lactulose, antibiotics, sodium benzoate

163
Q

What exam findings may be present in hepatic encephalopathy?

A

Sleep disturbance, mood change, disorientation, confusion
Asterixis, slurring, ataxia, hyperreflexia
Coma

164
Q

What is an initial lab difference between hepatocellular injury and cholestatic injury?

A

Hepatocellular: initial ALT elevation
Cholestatic: initial ALP elevation

165
Q

How can NASH disease be confirmed (non-invasively)?

A

Ultrasound showing fatty infiltrate

166
Q

How do you treat acetaminophen toxicity?

A

N-acetylcysteine

167
Q

What clinical features of hemochromatosis?

A 
Cirrhosis
Secondary diabetes
Bronze skin
Cardiac arrhythmias
Gonadal dysfunction

Increased risk of hepatocelluar carcinoma

168
Q

What causes Wilson’s disease?

A

Autosomal recessive ATP7B gene mutation

Defective ATP-mediated copper transport (Ceruloplasmin low/absent copper)

Copper overload in hepatocytes –> serum –> tissues –> free radical damage

169
Q

How are these transmitted?
Hepatitis A?
Hepatitis B?
Hepatitis C?

A

A: fecal oral
B: Blood, SEX, perinatal
C: Blood

170
Q

What are transaminases? What do they do?

Where are they found?

A

AST, ALT

Metabolize amino acids to synthesize proteins

AST = liver specific but not predictive of damage/disease

ALT = liver, skeletal muscle, RBCs, kidney, brain

171
Q

What substances are made in the liver?

A

Prothrombin, Albumin

Bilirubin (10% direct, conj in liver)

172
Q

What patterns of transaminitis would be seen in acute and chronic hepatitis?

A

Acute: AST/ALT >1000
Chronic: ALT/AST

173
Q

What might be suggested by AST & ALT >1000?

A

Toxins
Shock Liver
Viral Hepatitis

174
Q

What disease is p-ANCA+, associated with IBD, has a ‘string of pearls’ imaging and ‘onion skin’ pathology, and has an increased risk of cholangiocarcinoma?

A

Primary Sclerosing Cholangitis
–> Increased ALP, GGT

(inflammation/fibrosis of intra/extrahepatic bile ducts)

175
Q

What disease is associated with ANA & antimitochondrial Ab, women 30-65, fatigue and pruritus?

A

Primary Biliary Cholangitis
–> Increased ALP, GGT

(granulomatous destruction of intrahepatic bile ducts)

176
Q

What disease is associated with ANA and anti-smooth muscle Ab?

A

Autoimmune hepatitis

–> More common in women, 80% present with cirrhosis, Patho = plasma cells + hypergammaglobulinemia

177
Q

What hepatic disease will have AFP elevation?

A

hepatocellular carcinoma

178
Q

What are risk factors for NASH?

A

obesity, diabetes, hypertriglyceridemia, metabolic syndrome, hypertension

179
Q

What is the disease progression of NASH?

A

Steatosis (trig accumulation) –> steatohepatitis (inflammation + hepatocellular necrosis) –> cirrhosis

180
Q

What lab values make up the MELD score?

What does the MELD score indicate?

A

serum bilirubin, INR, serum creatinine

3-month mortality, different for inpatient v outpatient

181
Q

What are common pathogens in spontaneous bacterial peritonitis?

A

E.coli, Klebsiella, Streptococcus, other gut flora

182
Q

What is the presentation of SBP?

A

fever, abdominal pain, encephalopathy, worsening clinical condition

183
Q

What is a complication of SBP?

A

hepatorenal syndrome

184
Q

When is paracentesis indicated?

A

new onset ascites, signs of SBP, clinical deterioration (with OR without current treatment for SBP), symptom relief

185
Q

How do you treat SBP? When do you offer prophylaxis?

A

Cefotaxime (3rd gen)
Albumin infusion

Prophylaxis if hospitalized with GI bleed, ascites protein is 2.5, prior SBP

186
Q

How do you treat ascites?

A 
Sodium restriction
Water restriction
Diuretics (spironolactone + furosemide)
Paracentesis if symptomatic
Albumin infusion if >5L on para.
187
Q

What is the most common cause of death in cirrhosis patients?

A

Variceal hemorrhage

188
Q

How do you treat an acute GI bleed (variceal hemorrhage)?

A

Stabilize (large bore IV)
Octreotide (vasoconstrict)
Ceftriaxone (SBP prophy)
Band ligation +/- TIPS

Prophy with propranolol

189
Q

How do you diagnose hepatorenal syndrome?

A

AKI, no response to volume challenge, diagnosis of exclusion if no other source of AKI

190
Q

What is the cause of hepatorenal syndrome?

A

Splanchnic arteries vasodilation, renal circulation vasoconstriction

191
Q

How do you treat hepatorenal syndrome?

A

Increase MAP by 10-15
ICU: norepi + albumin
Non-ICU: octreotide, midodrine, albumin
TIPS + dialysis

192
Q

This is the most common acute viral hepatitis, diagnosed with IgM, for which there is a vaccine?

A

Hepatitis A

193
Q

These viral hepatitis viruses are (+) RNA

A

Hepatitis A, C and E

194
Q

These types of viral hepatitis are associated with cancer development

A

Hepatitis B (even without cirrhosis), Hepatitis C

195
Q

How do you treat Wilson disease?

A

D-penicillamine (chelator)

196
Q

Which viral hepatitis is the most common chronic form, but 20-40% of infections resolve?

A

Hepatitis C

197
Q

What does each of these indicate?

HBsAg
HBeAg
Anti-HBe
Anti-HBc
Anti-HBs
A 
HBsAg --> infection
HBeAg --> HIGH infectivity
Anti-HBe --> low infectivity
Anti-HBc --> chronic phase
Anti-HBs --> resolved/immune
198
Q

How do you diagnose hemochromatosis?

A

Presents late adulthood–>

Increased ferritin, Increased transferrin saturation (>45%)
HFE genotyping
Liver biopsy +/-

Increased risk of hepatocellular carcinoma

199
Q

What is shown on hemochromatosis biopsy?

A

Brown pigment in hepatocytes
Lipofuscin stains brown –> aging
Prussian blue stain distinguishes Fe (blue) from lipofuscin (brown)

200
Q

Macrolide antibiotics

Include:
Cover:
Mechanism:

A

Erythromycin‎
Azithromycin
Clarithromycin‎

Cover: Gram + , some Gram -

Mechanism: protein synthesis inhibitors

201
Q

Fluoroquinolone antibiotics

Include:
Cover:
Mechanism:

A 
ciprofloxacin 
gemifloxacin 
levofloxacin 
moxifloxacin 
norfloxacin 
ofloxacin

Cover BROAD spectrum gram + and gram -

Mechanism: topoisomerase inhibition

202
Q

What would you call impaired renal tubule acidification caused by the inability to excrete acid leading to hyperchloremic metabolic acidosis?

A

Type I Distal RTA

203
Q

What would you call impaired renal tubule acidification caused by reduced capacity to reclaim filtered bicarb leading to hyperchloremic metabolic acidosis?

A

Type II Proximal RTA

204
Q

What are common causes of Type I RTA?

A

Autoimmune (Sjogrens, RA)
Hypercalciuria
Hereditary
Drugs (Ifosfamide, Ibuprofen)

205
Q

What is the Anion Gap in RTA? Why?

A

Normal -

low serum bicarbonate, high chloride

206
Q

What will the urine pH be in RTA?

A

Type I - Distal - 5.5 or higher (normal) d/t progressive

Type II - Proximal - usually less than 5.3

207
Q

When might you see Type IV RTA?

A

In DM

208
Q

Nephritic Syndromes are due to…

A

glomerular basement membrane dysfunction

NephrItic –> Inflammation –> hematuria, RBC casts

209
Q

Podocyte disruption leading to impaired charge barrier and proteinuria are grouped as…

A

Nephrotic syndromes

210
Q

These are severe nephritic syndromes that most commonly produce nephrotic range proteinuria >3.5g/day (2)

A

Diffuse proliferative glomerulonephritis

Membranoproliferative glomerulonephritis

211
Q

IgG, IgM, C3 deposition along the GBM
Most commonly seen in children 1-3 weeks p infection
Resolved spontaneously
“cola colored urine” with hematuria and RBC casts
“starry sky” appearance on Immunofluorescence

A

Acute poststreptococcal glomerulonephritis
(nephrItic –> Inflammation)

1-3 weeks following GAS infection of pharynx or skin

212
Q

Renal insufficiency or URI or acute gastroenteritis
Episodic hematuria with RBC casts
Caused by immune complex deposits in mesangium

A

IgA nephropathy

2-4 days after mucosal infection (URI or gastroenteritis)

213
Q

What is the pathology of acute tubular necrosis?

A

Ischemic OR nephrotoxic injury

  • Ischemic: low blood flow, death of tubular cells
  • – PCT and thick ascending limb highly susceptible
  • Nephrotoxic: substances, crush injury or hemoglobinuria
  • – PCT susceptible
214
Q

What are the three stages of ATN?

A

Inciting event (injury)

Maintenance phase (oliguric 1-3w, high risk hyperK, met acidosis, uremia)

Recovery phase: polyuric, BUN/Cr fall, risk hypoK

215
Q

This may present with nephritis (eosinophilic casts), fever, rash & costavertebral tenderness OR may be asymptomatic

A

Drug-induced interstitial nephritis

  • -> May be weeks or even months after drugs
  • -> diuretics, penicillin, PPIs, sulfas, rifampin, NSAIDs
216
Q

Hematuria, normal serum complement and anti-GBM antibodies

A

Goodpasture syndrome/anti-GBM disease: test for

217
Q

Hematuria, normal serum complement and C-ANCA positive

A

Wegener’s Granulomatosis

218
Q

Hematuria, normal serum complement and P-ANCA positive

A

May be Microscopic polyangitis or Churg-Strauss syndrome

219
Q

What is the most common cause of death in cirrhosis patients?

A

Variceal hemorrhage

1/3 patients have variceal hemorrhage, each episode 30% mortality

220
Q

What is hepatorenal syndrome?

A

Vasodilation of splanchnic arteries (portal HTN, SBP) and vasoconstriction of renal circulation

221
Q

If high conjugated bilirubin, high alk phos, high ggt, low urine urobilirubin with dark urine and pale stool and pruritis?

A

Biliary tract obstruction

222
Q

What are the clinical features of cirrhosis?

A

Portal hypertension: ascites, splenomegaly, hepatorenal syndrome
Increased ammonia: mental status change, asterixis, coma
Increased estrogen: gynecomastia, spider angiomata, palmar erythema
Jaundice
Hypoalbuminemia: nephrotic syndrome, edema
Coagulopathy: bleeding disorder, monitor with PT

223
Q

What pattern of hepatic damage would be seen in:

Viral/autoimmune/hemochromatosis?

Alcoholic/NASH/vascular?

A

Viral/autoimmune/hemochromatosis –> periportal

Alcoholic/NASH/vascular –> central vein

224
Q

How do you treat hepatorenal syndrome?

A

Increase MAP by 10-15
In ICU: norepinephrine and albumin
Not in ICU: octreotide and midodrine and albumin

If unresponsive to medical therapy, TIPS and dialysis

225
Q

What are the indications for SBP prophylaxis?

A

Hospitalized cirrhosis with GI bleed
Ascites protein 2.5
Prior SBP

226
Q

What are the complications of cirrhosis?

A

1) ascites and SBP
2) variceal hemorrhage
3) hepatic encephalopathy
4) hepatorenal syndrome

227
Q

What is the first line therapy for peptic ulcer disease?

A

Triple therapy: PPI, Clarithromycin, Amoxicillin (or metro)

228
Q

What is the TIMI score and what do the values indicate?

A

Risk stratification of patients with NSTEMI or unstable angina

  • risk of death
  • risk of ischemic events
  • basis for therapeutic decision making

Score 0-2 –> meds, stress test –> angiography?
3 –> meds, early coronary angiography (before stress test)

229
Q

What are the complications of MI?

0-24hr
1-4d
3-14d
2-10w

A

0-24hr: arrhythmia, cardiogenic shock, HF, acute valve dysfunction
1-4d: pericarditis
3-14d: rupture, pseudoaneurysm
2-10w: Dressler (immune mediated pericarditis), true aneurysm

230
Q

What do Q-waves on an EKG indicate?

A

Necrotic tissue, may be 24-36hr after infarct

231
Q

What are the long-term outcomes of RCA infarct vs LCA infarct?

A

RCA usually has improved function due to less oxygen demand than LCA, smaller muscle mass, lower afterload, better coronary perfusion (occurs during diastole and systole), better collateral flow from LCAs.

232
Q

A patient presents with recurrent chest pain that occurs at rest, sometimes in the middle of the night and lasts for 10 minutes at a time. What is the likely diagnosis?

A

Prinzmetal angina

Dx with transient ST elevation during pain without high grade coronary stenosis

233
Q

What are the risk factors for nosocomial infections?

A

External instruments, age extremes, malnutrition, smoking, immunosuppression, depressed consciousness, wounds, burns, trauma, ICU, length of stay, prior antibiotics

234
Q

In what settings might you see Klebsiella pneumonia?

A

Alcoholics
Aspiration
HAP/HCAP

235
Q

In what setting might you see Legionella pneumonia?

A

Elderly
Smokers
TNF inhibition

236
Q

In what setting might you find Chlamydia pneumonia?

A

Young people

Community-acquired

237
Q

What patients might present with encapsulated bacterial pneumonia?

A

Post-splenectomy patients

238
Q

What are possible causes of hypernatremia when urine osmolality is low (60 or lower)?

A

Diabetes insipidus

239
Q

What are the risk factors for nosocomial infections?

A

External instruments, age extremes, malnutrition, smoking, immunosuppression, depressed consciousness, wounds, burns, trauma, ICU, length of stay, prior antibiotics

240
Q

In what settings might you see Klebsiella pneumonia?

A

Alcoholics
Aspiration
HAP/HCAP

241
Q

In what setting might you see Legionella pneumonia?

A

Elderly
Smokers
TNF inhibition

242
Q

In what setting might you find Chlamydia pneumonia?

A

Young people

Community-acquired

243
Q

What patients might present with encapsulated bacterial pneumonia?

A

Post-splenectomy patients

244
Q

What are possible causes of hypernatremia when urine osmolality is low (60 or lower)?

A

Diabetes insipidus

245
Q

What are common causes of respiratory alkalosis?

A 
Hyperventilation:
Hysteria
Hypoxemia (high altitude)
Salicylates (aspirin - early after ingestion)
Tumor
Pulmonary Embolism
246
Q

What are common causes of respiratory acidosis?

A

Hypoventilation (airway obstruction, COPD, other acute/chronic lung disease, opioids, sedatives, weak resp muscles)

247
Q

How is metabolic acidosis compensated for?

A

Metabolic acidosis = low pH, low bicarb, low PCO2
Compensate with hyperventilation

Next step: Check Anion Gap

248
Q

What are common causes of metabolic alkalosis?

A 
With compensation --> hypoventilation:
Loop diuretics
Vomiting
Antacid use
Hyperaldosteronism
249
Q

What is the mnemonic for HIGH Anion Gap Metabolic Acidosis?

A 
MUDPILES
Methanol 
Uremia
DKA
Propylene glycol
Iron tablets or INH
Lactic acidosis
Ethylene glycol
Salicylates
250
Q

What is the mnemonic for NORMAL Anion Gap Metabolic Acidosis?

A 
HARD-ASS
Hyperalimentation
Addison disease
RTA
Diarrhea
Acetazolamide
Spironolactone
Saline Infusion
251
Q

If a patient is tachypneic, he likely has this acid-base disorder

A

Respiratory alkalosis

Tachypnea –> Hyperventilation

252
Q

If a patient has impaired gas exchange in the lung (from obstruction, oversedation, etc) he likely has this acid-base disorder

A

Respiratory acidosis

Increased carbon dioxide concentration in blood

253
Q

If a patient has nausea and vomiting, and possibly low chloride, he likely has this acid-base disorder

A

Metabolic alkalosis

low plasma chloride + increased plasma bicarb

254
Q

If a patient is using diuretics, he likely has this acid-base disorder

A

Chloride depletion metabolic alkalosis

255
Q

If a patient has diarrhea, he likely has this acid-base disorder

A

Metabolic Acidosis (NORMAL anion gap)

Direct bicarbonate loss from the gut

256
Q

If a patient has chronic renal insufficiency, he likely has this acid-base disorder

A

Metabolic acidosis

Mild-mod –> Normal AG
Severe –> High AG

257
Q

If a patient has T1DM without insulin (DKA), he likely has this acid-base disorder

A

High AG Metabolic Acidosis

258
Q

If a patient has circulatory shock (anaerobic metabolism), he likely has this present

A

lactic acidosis –> increased plasma anion gap

Internal Medicine Core (1 decks)

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