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Step 2 Material > UWORLD + Step 2 > Flashcards

UWORLD + Step 2 Flashcards

1
Q

What is the best predictor of survival for STEMI?

A

Left ventricular EF

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2
Q

What is the treatment for STEMI?

A

MONA + H

Morphine
Oxygen
Nitrogen
Aspirin

Heparin

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3
Q

What is an ST-Elevation Myocardial Infarction (STEMI)?

A

ST-segment elevations and cardiac enzyme rlease secondary to prolonged cardiac ischemia and necrosis

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4
Q

What is the treatment for NSTEMI?

A

ABNHS

Aspirin
Beta-blocker
Nitrates
Heparin
Statin

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5
Q

What is an NSTEMI?

A

Indicates myocardial necrosis marked by elevation in tropinin I and CK-MB without ST-segment elevations seen on ECG

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6
Q

What is unstable angina?

A

The onset of new chest pain, accelerating or occurs at rest

Signals presence of possible impending infarction based on plaque instability

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7
Q

What are treatments for Angina Pectoris?

A

ASA
Oxygen
IV Nitroglycerin
IV Morphine
IV Beta-blocker

Can also use:
- CCBs (Diltazem, verapamil)
- ACEIs

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8
Q

What medications are shown to have a mortality benefits in the treatment of angina?

A

ASA and B-blockers

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9
Q

Classic Triad of Angina Pectoris?

A
  • Substernal chest pain
  • precipitated by stress or exertion
  • relieved by rest or nitrates
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10
Q

What is Prinzmetal’s (Variant) Angina?

A

Vasospasm of coronary artery which resembels agina pectoris

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11
Q

What is Angina Pectoris?

A

Substernal chest pain secondary to myocardial isschemia

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12
Q

What are the risk factors for CAD?

A

Age (males >45; females >55)
Male Gender
Increased LDL
Decreased HDL
Diabetes M.
Hypertension
Family Hx
Smoking
Peripheral arterial disease

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13
Q

A woman with hypertension and prior MI has an examination notable for displaced PMI, an S3, a nonelevated JVP, and bibasilar rales.

What is the next best step in diagnosis?

A

Dilated cardiomyopathy

An echocardiogram would be the next best diagnostic step

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14
Q

What is the side effect of Osmotic agents (diuretics)?

A
  • Pulmonary Edema
  • Dehydration
  • Contraindicated in anuria and CHF
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15
Q

What is the mechanism of action for Osmotic Agents (diuretics)?

A
  • Creates increased tubular fluid osmolarity
  • leading to increased urine flow
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16
Q

What are the sides effects of Carbonic Anhydrase Inhibitors?

A
  • Hypercholemic metabolic acidosis
  • Neuropathy
  • Ammonium Toxicity
  • Sulfa allergy
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17
Q

What is an example of an Osmotic agent?

A

Mannitol

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18
Q

What are examples of Carbonic Anhydrase Inhibitors?

A

Acetazolamide

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19
Q

What is the mechanism of action for Carbonic Anhydrase Inhibitors?

A

NaHCO3

Diuresis decreases total body NaHCO3

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20
Q

What are the side effects of K+ sparring agents?

A

Hyperkalemia
Gynecomastia
Sexual Dysfunction

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21
Q

What is the mechanism of action for K+ sparring diuretics?

A

Spironolactone:
- aldosterone receptor antagonist

Amiloride:
- block Na+ channels

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22
Q

What are some examples of potassium (K+) sparring diuretics?

A

Spironolactone
Amiloride

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23
Q

Side effects of thiazide diuretics?

A

Hypokalemia
Metabolic Alkalosis
Hyponatremia

and

Hyper[GLUC]
Hyperglycaemia
Hyperlipidemia
HyperUricemia
Hypercalcemia

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24
Q

Mechanism of action for Thiazide diuretics?

A

Decrease NaCl reabsorption
causes decrease the diluting capacity of the nephron
decrease calcium excretion

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25
Q

Example of Thiazide Diuretic?

A

HCTZ, Clorothiazide, chlorothalidone

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26
Q

What is the mechanism of action for Loop Diuretics?

A

Decrease Na/K/2Cl cotransporter
decrease urine concentration
increase calcium excretion

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27
Q

What are the side effects of Loop Diuretics?

A

Ototoxicity
hypokalemia
hypocalcemia
dehydration
gout

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28
Q

What are 4 Loop diuretics?

A

Furosemide
ethacrynic
bumetanide
torsemide

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29
Q

What medication should you avoid in CHF?

A

CCBs

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30
Q

What to provide for acute CHF management?

A

LMNOP

Lasix
Morphine
Nitrates
Oxygen
Position (Upright)

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31
Q

A patient with CHF, already on furosemide and metropolol, has an exacerbation. What is the next step in management?

A

Add ACEi.

had been shown to provide mortality benefits when used with B-blocker (NYHA II-IV)

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32
Q

What are acute causes of atrial fibrillation?

A

PIRATES

pulmonary disease
Ischemia
Rheumatic disease
Anemia
Thyrotoxicosis
Ethanol
Sepsis

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33
Q

How is the diagnosis of Primary Adrenal Insufficiency made?

A

The diagnosis of PAI is made by stimulation testing with cosyntropin, a synthetic form of ACTH. Low production of cortisol following cosyntropin administration is diagnostic of PAI.

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34
Q

What can Primary Adrenal Insufficiency Cause?

A

Mineralocorticoid deficiency causes renal salt wasting, with hypotension, weight loss, hyponatremia, hyperkalemia, and dietary salt craving.

Glucocorticoid deficiency leads to fatigue, anorexia, and many psychiatric manifestations of adrenal insufficiency (eg, irritability, and depressed mood). It also contributes to hypotension.

Androgen deficiency leads to loss of libido and suppression of secondary sexual characteristics (eg, reduced pubic hair). These effects are typically only seen in women because androgen production still occurs in the testes of men.

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35
Q

What causes Primary Adrenal Insufficiency?

A

PAI usually results from autoimmune destruction of the bilateral adrenal cortex

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36
Q

What are the zones of the adrenal gland and the hormone that they secrete + function?)

A

Zona Glomerulosa - Aldosterone
Zona Fasciculata - Cortisol
Zona Reticularis - Androgens

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37
Q

What is the most common cause of Hyperprolactinemia in child-bearing-age women? And what is the most appropriate next step to evaluate them?

A

Prolactinomas are the most common cause of hyperprolactinemia in women of reproductive age.

Therefore, the most appropriate next step in evaluating this patient is an MRI of the head.

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38
Q

What do mild elevations in prolactin (<200 ng/mL) suggest the cause to be?

A

Mild to moderate elevations (<200 ng/mL), can occur due to disruption of inhibitory dopamine pathways by medications (ie, antipsychotics [eg, haloperidol] but not usually selective serotonin reuptake inhibitors [eg, citalopram]).

They may also occur due to small prolactinomas (microadenomas) that may not present with classic mass symptoms (eg, headache, bitemporal hemianopsia)

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39
Q

What do moderate prolactin levels suggest the cause be?

A

Moderate hyperprolactinemia can be due to hypothyroidism or renal insufficiency, which are less likely in a patient with normal TSH and creatinine levels.

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40
Q

What do very high prolactin levels (eg, ≥200 ng/mL) suggest the cause to be?

A

Very high prolactin levels (eg, ≥200 ng/mL) usually indicate a prolactin-secreting pituitary macroadenoma (ie, prolactinoma or lactotroph adenoma).

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41
Q

What is a good hint about the cause of the Hyperprolactinemia?

A

The degree of hyperprolactinemia often correlates with the underlying cause

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42
Q

What do high prolactin levels cause?

A

High prolactin levels suppress hypothalamic GnRH secretion, leading to decreased LH and estradiol secretion.

The resultant hypogonadism presents clinically with oligomenorrhea/amenorrhea and anovulatory infertility

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43
Q

Clinical manifestations of Hyperprolactinemia?

A

Premenopausal women: oligomenorrhea/amenorrhea, infertility, galactorrhea

Postmenopausal women: mass effect symptoms (eg, headache, visual field defects) if due to large adenoma

Men: hypogonadism (decreased libido, erectile dysfunction), mass effect symptoms

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44
Q

Causes of Hyperprolactemia?

A

Physiologic (eg, pregnancy, breastfeeding)
Chest wall injury (eg, burns, herpes zoster)
Prolactinoma
Infiltrative pituitary/hypothalamic disorders (eg, malignancy, sarcoidosis)
Medications (eg, antipsychotics, metoclopramide)
Hypothyroidism
Chronic kidney disease

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45
Q

How do you evaluate Hyperprolactinemia?

A

Serum prolactin
MRI of the pituitary (if cause not known)

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46
Q

In a patient with hypertension, when should Renal Artery Stenosis be suspected?

A

Renal artery stenosis should be suspected in patients with
resistant hypertension,
recurrent flash pulmonary edema,
abdominal bruit,
or acute kidney injury after initiation of an ACE inhibitor.

It is most common in older adults with widespread atherosclerotic disease and young women with fibromuscular dysplasia but would be unlikely in this younger man with mild hypertension.

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47
Q

Who should be screened for an intracranial aneurysm?

A

Screening for intracranial aneurysms is recommended by some experts for patients with autosomal dominant polycystic kidney disease or with a family history of aneurysms in ≥2 first-degree relatives. Screening in the general population is not recommended.

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48
Q

Who should be screened for AAA?

A

Screening for abdominal aortic aneurysm with a one-time abdominal ultrasound is recommended for men aged 65-75 who have ever smoked.

Screening may also benefit men aged 65-75 who have not smoked but have other significant risk factors (eg, first-degree family history of abdominal aortic aneurysm rupture).

Screening in younger men and in women has little benefit and is not recommended.

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49
Q

What are the potential complications of an MI?

A

Papillary Muscle Rupture/Dysfunction
Interventricular septum rupture
Free wall rupture
Left Ventricular Aneurysm

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50
Q

What is Dressler’s Syndrome?

A

Post-cardiac injury syndrome (Dressler syndrome) is an immune-mediated pericarditis that may occur several weeks or months following MI, often with accompanying pericardial effusion

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51
Q

What are the indications for testing for pheochromocytoma in hypertensive patients?

A
  • resistant hypertension (ie, sustained hypertension despite an appropriate 3-drug treatment regimen);
  • episodic,
  • severe hypertension, especially when associated with adrenergic symptoms (eg, diaphoresis, tachycardia);
  • adrenal incidentaloma noted on imaging; and - hypertension in a patient with a family history of pheochromocytoma or multiple endocrine neoplasia
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52
Q

What is the definition of hypertension?

A

sustained blood pressure ≥130 mm Hg systolic or ≥80 diastolic

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53
Q

What are labratory evaluations of hypertension?

A

Renal function tests
- Serum electrolytes (Na, K, Ca)
- Serum creatinine
- Urinalysis
- Urine albumin/creatinine ratio (optional)

Endocrine tests
- Fasting glucose or hemoglobin A1c
- Lipid profile
- TSH

Cardiac tests
- ECG
- Echocardiography (optional)

Other tests
- Complete blood count
- Uric acid (optional)

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54
Q

What is hypertrophic Cardiomyopathy?

A

Impaired left ventricular relaxation and filling (nonsystolic function) due to thickened ventricular walls

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55
Q

What does an S4 Gallop Signify?

A

A stiff, noncompliant ventricle and increased “atrial kick” and may be associated with hypertrophic cardiomyopathy

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56
Q

What is the treatment for Hypertrophic Cardiomyopathy?

A

Beta-blockers are initial therapy for symptomatic relief; CCBs are second-line agents.

Surgical options include:
- dual-chamber pacing,
- partial excision or alcohol ablation of the myocardial septum,
- ICD placement,
- mitral valve replacement

Patients should avoid intense athletic competition and training

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56
Q

What is Restrictive Cardiomyopathy?

A

decreased elasticity of the myocardium leading to impaired diastolic filling (without significant systolic dysfunction)

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57
Q

What causes Restrictive Cardiomyopathy?

A

Infiltrative Disease (Amyloidosis, Sarcoidosis, Hemochromatosis)

OR

Scarring and Fibrosis (2* to radiation)

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58
Q

What is the treatment for Restrictive Cardiomyopathy?

A

Therapies are limited and are generally palliative only.
Include:
- Cautious use of diuretics for fluid overload
- Vasodilators to decrease filling pressure

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59
Q

What is the most common complication following acute MI?

A

Arrhythmia; with lethal arrhythmia is being the most frequent cause of death

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60
Q

What are less common complications of an MI?

A
  • Reinfarction
  • Left Ventricular wall rupture
  • Ventricular Septal Defect
  • Pericarditis
  • Papillary muscle rupture (w/ Mitral regurgitation)
  • Left Ventricular Aneurysm or pseudoaneurysm
  • Mural thrombi
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61
Q

What is Dyslipidemia?

A

Total Cholesterol level >200 mg/dL, LDL >130 mg/dL, Triglycerides >150 mg/dL, and HDL <40 mg/dL

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62
Q

What are some causes of Dyslipidemia?

A
  • Obesity
  • DM
  • Alcoholism
  • Hypothyroidism
  • Nephrotic Syndrome
  • Hepatic Disease
  • Cushing’s Syndrome
  • OCP use
  • High-dose diuretic use
  • Familial hypercholesterolemia
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63
Q

What is Hypertension?

A

Systolic BP >140 mmHg and/or diastolic BP >90 mmHg (based on 3 measurements separated in time)

Either 1* (Primary/Essential) or 2* (Secondary)

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64
Q

What are Statins?

A

HMG-CoA reductase Inhibitors

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65
Q

What is the mechanism of action for Statins?

A

inhibit cholesterol synthesis

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66
Q

What are the side effects of Statins?

A
  • Increased LFTs
  • Myositis (Inflammation of the muscle)
    -Warfarin Potentiation (the effect of warfarin, an anticoagulant medication, is increased or potentiated by another drug or substance)
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67
Q

What are fibrates? and provide an example?

A

Lipoprotein Lipase Simulators

Gemfibrozil

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68
Q

What is the mechanism of action for Fibrates?

A

Increase lipoprotein lipase leading to an increase in vLDL and triglyceride catabolism

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69
Q

What are side effects of Fibrates?

A
  • Upset GI
  • Cholelithiasis
  • Myositis
  • Increased LFTs
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70
Q

What is an example of a Cholesterol Absorption inhibitor?

A

Ezetimibe (Zetia)

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71
Q

What is the Mechanism of Action for Ezetimibe (Zetia)?

A

Decreased absorption of cholesterol at the small intestine brush border

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72
Q

What are the side effects of Ezetimibe (Zetia)?

A
  • Diarrhea
  • Abdominal Pain
  • Can cause angioedema
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73
Q

What is the Mechanism of Action for Niaspan?

A
  • Decreased fatty acid release from adipose tissue
  • Decreased hepatic synthesis of LDL
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74
Q

What are the side effects of Niaspan (Niacin)?

A
  • Skin flushing (can be prevented with ASA)
  • Paresthesias
  • Pruritus
  • GI Upset
  • Increased LFTs
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75
Q

What are some examples of Bile acid resins?

A
  • Cholestyramine
  • Colestipol
  • Colesevelam
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76
Q

What is the Mechanism of Action of Bile Acid Resins?

A

Bind intestinal bile acids, leading to:
(1) decrease bile acid stores
(2) Increased catabolism of LDL from plasma

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77
Q

What are the side effects of Bile Salt Resins?

A
  • Constipation
  • GI Upset
  • LFT abnormalities
  • Myalgias
  • Can decrease absorption of other drugs from the small intestine
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78
Q

What is the treatment of Hypertension?

A

ABCD

ACEi’s/ARBs
Beta-Blockers
CCBs
Diuretics

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79
Q

What are some causes of 2* (secondary) Hypertension?

A

CHAPS

Cushing’s Syndrome
Hyperaldosteronism (Conn’s Syndrome)
Aortic Coarctation
Pheochromocytoma
Stenosis of renal arteries

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80
Q

What is the treatment of 1* (primary renal disease) causing hypertension?

A
  • Treat with ACEi’s

This slows the progression of renal disease

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81
Q

What is the treatment of Pheochromocytoma (causing hypertension)?

A

Diagnose with urinary metanephrine & catecholamine levels or plasma metanephrine

Surgical removal of tumour after treatment w/ both:
(1) Alpha-blockers
(2) Beta-blockers

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82
Q

What is the treatment of Conn’s Syndrome (causing hypertension)?

A
  • Metabolic workup w/ plasma aldosterone & Renin levels
  • Increased Aldosterone and decreased renin suggest 1* (primary) Hyperaldosteronism
  • Surgical Removal of Tumor
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83
Q

What is the treatment of Cushing’s Syndrome (Causing Hypertension)?

A
  • Surgical removal of tumour
  • Removal of exogenous steroids
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84
Q

What is the treatment of Coarctation of the aorta (causing hypertension)?

A
  • Surgical Repair
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85
Q

What is hypertensive urgency?

A

Elevated BP with mild to moderate symptoms (headache, chest pain)

WITHOUT end-organ damage

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86
Q

What is Hypertensive emergency?

A

Elevated BP WITH signs or symptoms of impending end-organ damage

(i.e., AKI, intracranial hemorrhage, papilledema, or ECG changes suggestive of ischemia or pulmonary edema)

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87
Q

What is the treatment for hypertensive urgencies?

A
  • Oral antihypertensives (i.e., beta-blockers, clonidine, ACEi’s)
    Goal: Gradually lower BO over 24-48 hours
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88
Q

What is the treatment for hypertensive emergencies?

A
  • Treat with IV medications (i.e., Labetaolol, Nitroprusside, Nicardipine)

Goal: Lowering mean arterial pressure by NO MORE than 25% over the first 2 hours

This is to prevent cerebral hypoperfusion or coronary insufficiency

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89
Q

What are some causes of Pericarditis?

A

CARDIAC RIND

Collagen Vascular Disease
Aortic Dissection
Radiation
Drugs
Infections
Acute renal Failure
Cardiac (MI)
Rheumatic Fever
Injury
Neoplasms
Dressler’s Syndrome

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90
Q

What is pericarditis?

A

Inflammation of the pericardial sac.

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91
Q

What ECG finding is consistent with Pericarditis?

A

Diffuse ST-segment elevation and PR-segment depressions

Which are followed by T-wave inversions

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92
Q

What is the most common cause of atypical pneumonia?

A

Mycoplasma Pneumoniae

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93
Q

What are the symptoms of Mycoplasma Pneumoniae?

A

Headache
Malaise
Fever
Incessant dry cough
Nonpurulent pharyngitis
Macular skin rash
subclinical hemolytic anemia

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94
Q

What is Empiric Treatment for Mycoplasma Pneumoniae?

A

oral antibiotics (i.e., Azithromycin, Doxycycline or Fluroquinolone - levofloxacin, moxifloxacin)

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95
Q

What is the most common cause of community-acquired pneumonia?

A

Streptococcus Pneumoniae

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96
Q

How does Streptococcus pneumoniae typically present?

A

Abruptly with fever
productive cough
dyspnea
lobar (NOT Interstitial) infiltrate on chest x-ray

Upper Respiratory Symptoms (i.e., Pharyngitis) and skin rash are uncommon.

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97
Q

What does Parvovirus B19 cause?

A

Influenza-like symptoms (i.e., Myalgias, fever, malaise)
Malar rash

Pulmonary symptoms and an interstitial infiltrate are not typical

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98
Q

What does Moraxella Catarrhalis cause?

A

Primarily Otitis Media (in Children)
Chronic Obstructive Pulmonary Disease (COPD) Exacerbations

An uncommon cause of pneumonia in healthy adults

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99
Q

What does Legionella Pneumophila cause?

A

high fever with prominent gastrointestinal (i.e., vomiting, diarrhea) & Systemic (i.e., headache, confusion, malaise) symptoms

Pulmonary Symptoms (i.e., Cough, Dyspnea) tend to evolve slowly over days.

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100
Q

How does Influenza Present?

A

Abrupt (i.e., Malaise, Myalgia, fever, headache)

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101
Q

How does Adolescent Idiopathic Scoliosis typically present?

A

In Asymptomatic children >10 years old

May include:
- rib bump
- asymmetric scapulae
- unilateral thoracic/lumbar prominence on forward bend test

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102
Q

What is the role of Spine X-ray in Adolescent Idiopathic Scoliosis?

A
  • Assess maturity
  • Measure the degree of curvature (i.e., Cobb Angle)
  • Rule out other deformities
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103
Q

What Cobb Angle is consistent with Scoliosis?

A

> 10 degrees

104
Q

What are risk factors associated with curve progression?

A

Female Sex
Age <12
Early Pubertal Status (i.e., Premenarchal)
Skeletal Immaturity
Severe curvature (i.e., Cobb angle > or = 25 degrees)

105
Q

When does Adolescent Idiopathic Scoliosis stop progressing?

A

Until growth and bone ossification are complete

106
Q

What questionnaire is used to quantify risk for Obstructive Sleep Apnea (OSA)?

A

STOP-Bang Questionnaire

107
Q

What symptoms do Obstructive Sleep Apnea patients present with?

A

Depressive symptoms:
- Fatigue
- Sleep Disturbances w/ multiple awakenings
- Impaired concentration
- Irritability
- Low mood

108
Q

How do you conform Obstructive Sleep Apnea?

A

Polysomnography demonstrating obstructive respiratory events

109
Q

What are appropriate treatments for Obstructive Sleep Apnea?

A

i.e., Positive Airway pressure, oral appliances

110
Q

What is Antiphospholipid-antibody Syndrome (APS)?

A

Prothrombotic autoimmune disorder caused by antiphospholipid antibodies (i.e., Anticardiolipin antibody, Lupus Anticoagulant)

111
Q

What do Antiphospholipid antibodies do?

A

disrupt function of platelets and vascular endothelial cells

Result in hypercoagulable state

112
Q

What are examples of initial presentation of Antiphospholipid-Antibody Syndrome (APS)?

A
  • Unprovoked arterial or venous thrombosis (i.e., stroke, DVP)

In pregnant patients:
- persistent thrombosis of placental vessels
- recurrent pregnancy losses

113
Q

What are the Diagnostic Criteria for Antiphospholipid-Antibody Syndrome?

A

1 Clinical & 1 Laboratory criterion must be met

114
Q

What are the potential clinical criterion for Antiphospholipid-antibody syndrome?

A

Vascular Thrombosis:
- Arterial or Venus

Pregnancy Morbidity:
- > or = 3 consecutive, unexplained fetal losses before the 10th week
- > or = 1 unexplained fetal losses after 10th week
- > or = 1 premature births of normal neonates before 34th week due: preeclampsia, eclampsia, or placental insufficiency

115
Q

What are the Laboratory criterion for Antiphospholipid-antibody syndrome?

A

Lupus anticoagulant
Anticardiolipin antibody
Anti-beta-2 glycoprotein antibody I

116
Q

What is the preferred anticoagulant therapy for Antiphospholipid-antibody Syndrome in pregnancy?

A

Low Molecular Weight Heparin (LMWH)

It is not associated with Teratogenicity

117
Q

What is Anterior Uveitis?

A

Inflammation of the anterior uveal tract (i.e., iris, ciliary body)

118
Q

How does Anterior Uveitis Present?

A

Symptoms:
- Ocular Pain
- Photophobia
- Decreased acuity

Examination:
- Ciliary Flush
- Pupillary Constriction
- hypopyon
- accumulation of white blood cells that form a
whitish layer of fluid in the lower portion of the eye’s
anterior chamber

119
Q

What are some common causes of Anterior uveitis?

A

Infections:
- Herpesviruses, Toxoplasmosis, Syphilis

Systemic Inflammtory Disorders:
- Sarcoidosis
- Spondylarthritis (i.e., Ankylosing spondylitis, reactive arthritis)
- Inflammatory Bowel Disease

120
Q

What some evaluations/tests for Anterior Uveitis?

A

Slit-Lamp Examination

HLA-B27 (Human Leukocyte Antigen B27)
Pelvis/Spine X-ray
Chest X-ray
HIV
Syphilis Serology

121
Q

What is the treatment for Anterior Uveitis?

A

Dilating eye drops (i.e., Cyclopentolate)
Topical Glucocorticoids

122
Q

What are Anti-Ro/SSA antibodies seen in?

A

Sjogren’s Syndrome

123
Q

What can be the two types of Diabetes Insipidus?

A

Central DI
Nephrogenic DI

124
Q

What are the causes of Central Diabetes Insipidus?

A

Decreased ADH secretion from the Pituitary

Usually has significant hypernatremia (>150 mEq/L)

125
Q

What is nephrogenic Diabetes Inspidius?

A

Normal ADH levels, with varying degrees of ADH resistance.

Have normal Sodium levels

126
Q

What is Acute Intermittent Porphyria (AIP)?

A

An autosomal dominant disorder involving alterations in enzymes involved in heme biosynthesis

Acute, intermittent neurovisceral attacks

127
Q

What is Wilson’s Disease?

A

accumulation of copper in the tissues - causing insidious hepatic, psychiatric, and neurologic dysfunction.

128
Q

What is the definition of the Mixed Connective TIssue Disease?

A

Autoimmune Disorder with variable features of:
- Systemic Lupus Erythematosus
- Systemic Sclerosis
- Polymyositis
- Rheumatoid Arthritis

129
Q

What are the clinical features of Mixed Connective Tissues Disease?

A
  • Raynaud Phenomenon
  • Hand/Finger Swelling (Diagnostic)
  • Arthritis/Synovitis (Diagnostic)
  • Inflammatory Myopathy (Diagnostic)
  • Pulmonary Hypertension
  • Malar or Discoid rash
  • Mild CNS &/or Kidney Disease
130
Q

What are the laboratory findings for Mixed Connective Tissue Disease?

A
  • Anti-U1 ribonucleoprotein
  • Antinuclear antibody
  • Rheumatoid factor, anti-cyclic citrullinated peptide
  • Elevated creatine kinase
  • Anemia/Cytopenia
131
Q

What are the treatments for Mixed Connective Tissue Disease?

A
  • Systemic Glucocorticoids
  • Corticosteroid-sparing agents (i.e., Methotrexate)
132
Q

What is Ankylosing Spondylitis characterized by?

A
  • Chronic back pain
  • loss of spinal mobility
  • Inflammation of ligamentous attachments
  • Associated with HLA-B27
133
Q

What does Granulomatosis with polyangiitis cause?

A
  • Multisystem vasculitis
  • prominent upper (i.e., nasal crusting, recurrent sinusitis)
  • Lower (i.e., cough, dyspnea) respiratory features
  • Positive antineutrophil cytoplasmic antibody.
134
Q

How can arthritis associated with IBD manifest?

A
  • As large-joint oligoarthritis
  • symmetric small-joint arthritis
  • Spondylarthritis
  • associated with HLA-B27 and HLA-DR103
135
Q

What are the clinical features of Essential Tremors?

A
  • Bilateral action tremor of hands
  • Head tremor without dystonia
  • No other neurologic signs
  • Improves with alcohol
136
Q

What are the clinical features of Parkinson’s Disease (Basal Ganglia Dysfunction) Tremors?

A
  • Resting tremor; decreases with voluntary movement
  • Pill-rolling
  • Asymmetric; hands & legs
137
Q

What are the clinical features of Cerebellar Tremors?

A
  • Usually associated with ataxia &/or dysmetria, nystagmus
  • Increases steadily as the hand approaches the target
138
Q

What are the clinical features of Orthostatic tremors?

A
  • effects on legs & trunk
  • Occurs only when standing; relieved by sitting
139
Q

What are the clinical features of Physiologic tremors?

A
  • Low amplitude, not visible under normal conditions
  • Increase sympathetic activity (i.e., Drugs, Hyperthyroidism, anxiety, caffeine)
  • worse with movement
  • Most common cause of tremors
140
Q

What is Herpes Zoster Virus?

A

Shingles; latent Varicella zoster virus infection

141
Q

What are the clinical features for Shingles?

A
  • Rash limited to a single dermatome
  • Associated neuritic symptoms (i.e., pain, itching, burning, and allodynia)
    • these may precede onset of visible rash
142
Q

What are two factors that can predispose people to shingles?

A

Age
Immunocompromised status

143
Q

What is the treatment for Shingles?

A

Antiviral agents (i.e., Acyclovir, famciclovir, valacyclovir) decrease the duration of symptoms + onset of post-herpetic neuralgia (especially if initiated within 72 hours)

144
Q

What is the clinical presentation for Pulmonary Embolism?

A
  • Pleuritic chest pain
  • Dyspnea
  • Tachypnea
  • Tachycardia
  • Cough
  • Hemoptysis
  • Lower extremity pain/swelling (i.e., Deep Vein Thrombosis)
145
Q

What are the chest x-ray signs highly suggestive for PE?

A
  • Westermark Sign:
    • Peripheral hyper lucency of the pulmonary arterial tree resulting from
      blood flow being cut off by the PE (focal Oligemia/hypervolemia)
  • Hampton Hump:
    • Peripheral, wedge-shaped lung opacity representing infarction.
  • Fleischner sign:
    • Enlargement of Pulmonary artery from increased pressure proximal to PE
146
Q

What are the clinical signs of Acute Decompensated Heart Failure?

A
  • Dyspnea
  • Orthopnea
  • S3 (From increased atrial pressure)
  • Distended Jugular Veins
  • Lung Crackles
  • Lower Extremity Edema
147
Q

What is the initial management for Acute Decompensated Heart Failure?

A
  • Evalue clinical Stability
  • Improve Symptoms
  • Investigate possible precipitating factors
148
Q

How do you evaluate stability in Acute Decompensated Heart Failure?

A
  • Ventilatory support (i.e., Respiratory Failure)
  • Inotropic support (i.e., Cardiogenic shock)
149
Q

How do you improve symptoms in Acute Decompensated Heart Failure?

A
  • Reducing preload with IV diuretics and venodilators (i.e., Nitroglycerin)
  • balanced venous and atrial dilator (i.e. Nitroprusside) may be given instead of venodilator when afterload reduction is also needed
150
Q

What are some possible precipitating factors to Acute Decompensated Heart Failure?

A
  • Myocardial infarction
  • Cardiac Arrhythmia
  • Severe Valvular Dysfunction
151
Q

What class of medications are Dobutamine and Milrinone?

A

Inotropic Medications

Help sustain adequate cardiac output by increasing cardiac contractility

152
Q

What is Tularemia?

A

uncommon infection caused by Francisella tularensis (highly virulent gram-negative coccobacillus)

153
Q

How is Tularemia transmitted?

A
  • Wild animals (i.e., Hare, rabbit) hunting/skinning
  • Tick or mosquito bite
  • bioterrorism agent
154
Q

What are the common manifestations of Tularemia?

A
  • Nonspecific: Fever, malaise
  • Ulceroglandular disease:
    • Single papuloulcerative lesion (sometimes absent)
    • Tender, supportive regional lymphadenopathy
  • Pneumonia
155
Q

What is the clinical manifestation of Carbon Monoxide Poisoning?

A

Anion Gap metabolic Acidosis (AGMA) due to lactic acidosis from peripheral tissue hypoxia

Mild-moderate:
- Headache, confusion
- Malaise, dizziness, nausea

Severe:
- Syncope, Seizure, Coma
- Myocardial ischemia, arrhythmias

156
Q

What is the treatment for Carbon Monoxide Poisoning?

A

High-flow 100% oxygen
Intubation/hyperbaric oxygen (severe)

157
Q

On MRI, what is a sign of permanent hypoxic brain injury?

A

Bilateral hyperintensity of the Globus pallidus (area highly sensitive to hypoxic conditions)

158
Q

For Duodenal Ulcers, when is the pain worse?

A

On an empty stomach (in contrast to Gastric Ulcers)

Possibly due to unopposed gastric acid emptying into the duodenum and improving with food (due to alkaline fluid secretion into the duodenum

159
Q

What are the major causes of Duodenal ulcers?

A

Helicobacter Pylori Infection
NSAIDs

NOTE: Malignant ulcerations should be considered with gastric ulcers; but are unlikely in young patients with Duodenal ulcers

160
Q

What is the treatment for patients with suspected H. Pylori-related Duodenal Ulcer?

A
  • Antisecretory Therapy: Preferably PPI (i.e., Omeprazole, pantoprazile) &
  • Antibiotic eradication: I.e., Amoxicillin + Clindamycin
161
Q

What is Selective Vagotomy?

A

Decreases gastric acid production by removing vagal input to the stomach

Used only in refractory cases

162
Q

What are the clinical features of Hyperosmolar Hyperglycemic State (HHS)?

A
  • Subacute or acute onset
  • Altered Mentation
  • Hyperglycemic symptoms (i.e., Polyuria)
  • Volume Depletion
163
Q

What are inciting factors for HHS?

A
  • Acute Illness, Trauma, Infection
  • Insulin nonadherence
  • Medications: Glucocorticoids, diuretics, atypical antipsychotics
164
Q

What are the laboratory studies for HHS?

A
  • Glucose >600 mg/dL (33.3 mmol/L)
  • Bicarbonate >18 mEq/L (18 mmol/L)
  • Normal anion gap
  • Negative or small serum ketones
  • Serum osmolality >320 mOsm/Kg (320 mmol/Kg)
165
Q

What is Priapism?

A

Prolonged, painful erection in the absence of ongoing sexual stimulation

166
Q

What is the pathogenesis of Priapism?

A
  • Impaired venous outflow from corpora cavernosa
  • Increased cavernosal pressure
  • Ischemia, hypoxia, acidosis
167
Q

What are some causes of Priapism?

A
  • Autonomic dysfunction: Spinal Cord Injury
  • Altered blood viscosity: Sickle cell disease, blood dyscrasias
  • Medications/Drugs: Phosphodiesterase inhibitors (i.e. Sildenafil), trazodone, stimulants
168
Q

What are the treatments for Priapism?

A
  • Aspiration, irrigation
  • Intracorporal alpha-1 adrenergic agonist (i.e., Phenylephrine)
169
Q

What are most cases of Priapism caused by?

A

Idiopathic

170
Q

What is the clinical features/Diagnosis of Uremic Pericarditis?

A
  • Pleuritic chest pain (decreased when sitting) +/- fever
  • Pericardial friction rub (highly specific)
  • ECG: Diffuse ST-segment elevations & PR-segment depression
  • Echocardiography: Pericardial Effusion
171
Q

What are some causes of Acute Pericarditis?

A
  • Viral or idiopathic
  • Autoimmune disease (i.e., SLE)
  • Uremia (Acute or chronic renal failure) (>60 mg/dL)
  • Post Myocardial Infarction
    • Early: Peri-infarction pericarditis
    • Late: Dressler Syndrome
172
Q

What is unique about Uremic pericarditis, compared to other causes?

A

Does not typically cause diffuse ST elevation (or PR depression) on ECG

As inflammation does not affect the myocardium

173
Q

Is dialysis indicated for Uremic pericarditis?

A

Yes; typically leads to resolution of symptoms

However, >50% of cases are accompanied by pericardial effusion, cardiac tamponade (which should be ruled out before initiating dialysis).

174
Q

What is the treatment for Acute Pericarditis?

A
  • NSAIDs & Colchicine for viral or idiopathic etiology
  • Variable for other etiology
175
Q

What is the origin location of Atrial Fibrillations?

A

Pulmonary Veins

176
Q

What is the origin location of Atrioventricular nodal reentrant tachycardia?

A

Atrioventricular node

177
Q

What is the origin location of Atrial flutter?

A

Cavotricuspid isthmus

178
Q

What is the origin location of AV reentrant Tachycardia

A

Bundle of Kent

179
Q

What is the origin location of Atrial tachycardia?

A

Ectopic pacemaker

180
Q

What does Focal Segmental Glomerulosclerosis result in?

A
  • Podocyte injury (foot process effacement on EM)
  • Loss of filtration barrier (usually causes Nephrotic Syndrome (i.e., Peripheral Edema, proteinuria >3.5 g/day)
181
Q

What is Primary FSGS?

A

a circulating factor causing podocyte injury, resulting in kidney dysfunction and nephrotic syndrome

However, immunofluorescence is typically negative.

182
Q

What is Secondary FSGS?

A

Podocyte injury from:
- Glomerular hyperfiltration (i.e., Severe obesity, solitary kidney)
- Toxins (i.e., Heroin)
- Infection (i.e., HIV)

Causing kidney dysfunction and proteinuria that may or may not reach nephrotic range

183
Q

What are the clinical features of Focal Segmental Glomerulosclerosis?

A
  • Primary: Usually Nephrotic Syndrome (Proteinuria >3.5 g/Day, Generalized Edema, hypoalbuminemia)
  • Secondary: Proteinuria +/- nephrotic syndrome
184
Q

What appears for the diagnosis of FSGS?

A

Light Microscopy: Segmental scarring in <50% of glomeruli

Immunofluorescence Microscopy: Usually Negative

Electron Microscopy: Podocyte foot process effacement

185
Q

What is the treatment for FSGS?

A
  • Renin-angiotensin blockade, loop diuretics
  • Primary FSGS: Immunosuppression
  • Secondary FSGS: Risk factor modification (i.e., Weight loss, ART)
186
Q

What are the clinical features of psoriatic arthritis?

A
  • Asymmetrical Arthritis
  • Soft tissue & Nail involvment
  • Skin lesions
187
Q

Describe the arthritis seen within psoriatic arthritis.

A
  • Distal Interphalangeal joints
  • Asymmetric oligoarthritis
  • Symmetric polyarthritis, similar to rheumatoid arthritis
  • Arthritis mutilans (deforming & destructive arthritis)
  • Spondylarthrities (sacroiliitis & spondylitis)
188
Q

Describe the Soft Tissue & Nail Changes seen in Psoriatic Arthritis.

A
  • Enthesitis (inflammation at the site of tendon insertion into bone)
  • Dactylitis (“Sausage digits”) of toe or finger
  • Nail pitting & Onycholysis
  • Swelling of the hands or feet with pitting edema
189
Q

Describe the skin lesions of psoriatic arthritis.

A
  • Arthritis precedes skin disease in 15%% of patients
  • Skin lesions are present but not yet diagnosed in 15% of patients
190
Q

What is Myotonic Dystrophy?

A
  • Autosomal dominant disorder
  • Most commonly caused by cytosine-thymine-guanine (CTG) trinucleotide repeat expansion in dystrophia myotonica protein kinase (DMPK) gene
191
Q

What is Myotonic Dystrophy characterized by?

A
  • Myotonia (Delayed muscle relaxation) w/ progressive muscle atrophy and weakness.
192
Q

What can facial muscle involvement for Myotonic Dystrophy present as?

A
  • ptosis and temporal wasting
  • flat affect (limited facial expression)
  • Eyelid myotonia (delayed ability to open eyes - after closing them tightly)
193
Q

What can distal musculature involvement for Myotonic Dystrophy present as?

A
  • Grip myotonia (i.e., Stiffness, Inability to release the hand grip)
194
Q

What are other characteristic features not associated with muscular involvement for Myotonic Dystrophy?

A
  • Cataracts
  • Frontal balding
  • Insulin resistance
  • Testicular atrophy
  • Sleep Disturbances (i.e., Hypersomnia, excessive daytime sleepiness)
195
Q

What is the presentation of Myotonic Dystrophy in childhood?

A

Cognitive & behavioural difficulties (class symptoms develop overtime)

196
Q

What is the presentation of Myotonic Dystrophy in infantile age?

A
  • Hypotonia
  • Respiratory failure
  • Inverted V-Shaped upper lip
197
Q

What are associated findings of Myotonic Dystrophy?

A
  • Cardiac: Arrhythmias, Cardiomyopathy
  • Gastrointestinal: Dysphagia, Constipation
  • Respiratory: Pharyngeal weakness, Hypoventilation
  • Nonmuscular: Insulin Resistence, hypogonadism, Cataracts, frontal balding, excessive daytime sleepiness
198
Q

What is the diagnosis & treatment for Myotonic Dystrophy?

A
  • Genetic testing
  • Supportive management
199
Q

What are the different TB skin Test Threshold for positive test?

A

> 5mm:
- Individuals with HIV infection
- Recent contacts of patient with known TB
- Persons with nodular or fibrotic changes on chest x-ray consistent with previously healed TB
- Organ transplant recipients & other immunosuppressed persons

> 10 mm:
- Recent immigrants (<5 years) from TB-endemic areas
- IV drug use
- Residents & employees in high-risk settings (i.e., prisons, nursing homes, etc.,)
- Mycobacteriology laboratory personal
- Persons w/ conditions that result in a higher risk for TB reactivation (i.e., DM, Leukemia, ESRD, Chronic malabsorption syndromes, Low body weight)
- Children aged <5 or those exposed to adults in high-risk categories

> 15mm: All of the above + healthy persons

200
Q

How can Jock Itch (Tinea Cruris) be confirmed?

A

Potassium hydroxide preparation of skin scrapings (especially in severe or atypical cases)

201
Q

What are effective treatment for Tinea Cruris?

A

Topical Antifungals
- i.e., Clotrimazole, Tolnaftate

Oral Antifungals
- i.e., Flucanazol (for severe or refractory cases)

202
Q

What are preventative measures for Tinea cruris?

A
  • Good hygiene w/ thorough drying
  • And/or Desiccant powders after bathing
203
Q

What do you do if you identify dermatophyte infection (ie., tinea pedis, corporis) with Tinea cruris?

A

should be identified and treated to prevent reinfection via autoinoculation

204
Q

What is Biliary Atresia?

A

Progressive and potentially fatal disease in which extrahepatic bile ducts become fibrosed and ultimately destroyed

205
Q

What is Bilirubin?

A

product of heme breakdown; normally conjugated in the liver and then transported through the bile ducts and gallbladder to the intestines for excretion in stool

206
Q

What is Kasai Procedure?

A

Hepatoportoenterostomy

Diverts bile to the small intestine and is most successfully performed before age 2 months;

Liver transplantation is often required

207
Q

What can untreated Biliary Atresia lead to?

A

Cirrhosis
Portal hypertension
Death

208
Q

What presentation suggests Renal Artery Stenosis?

A

HTN-related symptoms:
- resistant HTN (uncontrolled despite 3-drug regimen)
- Malignant HTN (w/ end-organ damage)
- Onset of severe HTN (>180/120 mmHg) after 55
- Severe HTN with Diffuse atherosclerosis
- Recurrent flash pulmonary edema with severe HTN

209
Q

What is supportive evidence for Renal Artery Stenosis?

A

Physical examination:
- Asymmetric renal size (>1.5 cm)
- Abdominal bruit

Laboratory results:
- Unexplained rise in serum creatinine (>30%) after starting ACE inhibitors or ARBs

Imaging results:
- Unexplained atrophic kidney

210
Q

What does renal ischemia, in Renal Artery Stenosis, activate?

A

Renin-angiotensin-aldosterone system

Causing:
- Sodium and water retention
- Generalized vasoconstriction
- Hypertension

211
Q

What do Laboratory abnormalities reflect in Renal Artery Stenosis?

A

Secondary Hyperaldosteronism (i.e., Hypokalemia, Elevated serum bicarbonate)

212
Q

How is the diagnosis of Renal Artery Stenosis confirmed?

A

With renal imaging (i.e., r enal ultrasound w/ doppler, CT/MR angiography)

213
Q

What is the management of Renal Artery Stenosis?

A
  • Blood pressure control
  • aggressive treatment of atherosclerotic disease (i.e., statins, smoking cessation)
  • ACE inhibitor (w/ close monitoring of renal function)
  • Revascularization
214
Q

What is the dexamethasone suppression test used for?

A

To identify Cushing Syndrome

Can cause hypertension; but typically associated with:
- Abnormal glucose tolerance
- Striae
- Easy brusing
- Obesity
- Enlarged dorsal fat pad
- NOTE: pulmonary edema is unexpected

215
Q

What is a common cause of anterior cord syndrome?

A
  • Injury to the Anterior spinal artery
    (i.e., Disc retropulsion, fragments of bone from vertebral burse fracture
216
Q

What are the neurological findings of Anterior Cord Syndrome?

A
  • Bilateral Hemiparesis (Lateral Corticospinal tract)
  • Diminished bilateral pain and temperature sensation (1-2 levels below the level of cord injury)
  • Intact bilateral proprioception, vibratory sensation, and light tough
217
Q

What are the symptoms of Diabetic Ketoacidosis?

A
  • Rapid onset weight loss
  • Polydipsia (increase thirst)
  • Diffuse abdominal pain (possibly from acidosis and electrolyte abnormalities impairing GI function - i.e., delayed gastric emptying, ileus, etc.,)
218
Q

What is the diagnosis of Diabetic Ketoacidosis?

A
  • Increased Glucose (300 - 800 mg/dL)
  • Metabolic Acidosis (bicarbonate <18 mEq/L)
  • Increased Anion gap
  • Positive serum ketones
219
Q

What is the treatment for Diabetic Ketoacidosis?

A
  • High-flow IV fluids (Normal Saline)
  • IV Insulin
  • Follow & replace potassium
220
Q

What is an Imperforate hymen?

A

Hymen fails to fenestrate during embryonic development

A common cause of primary amenorrhea

221
Q

What is the doctrine of double effect?

A

Related to terminal illness

interventions that have adverse effects are justified if they are given with the intention of:
1. Promoting the patient’s well-being OR
2. allowing for a comfortable death

222
Q

What do Nitrates do?

A

Primarily vasodilators - Dilate veins, arterioles, and coronary arteries by relaxing vascular smooth muscles

However, Primary anti-ischemic effects due to systemic vasodilation rather than coronary vasodilation

223
Q

What does Systemic venodilation cause on preload?

A

Lowers preload and left ventricular end-diastolic volume

Reduces myocardial oxygen demand by reducing wall stress

224
Q

Where do most SCC arise in the lungs?

A

Central portion of the lung (i.e., Hilar Mass)

Due to squamous metaplasia –> Dysplasia –> carcinoma In-situ within central tracheobronchial tree

225
Q

How do patients with SCC of the lungs present?

A
  • Cough
  • Dyspnea
  • and/or Hemoptysis (due to erosion of airway mucosa)
226
Q

Why is SCC associated with Hypercalcemia of malignancy?

A

Due to release of PTH-related protein (PTHrP)

Binds to PTH receptor on bones and in distal tubule of the kidney
- increases calcium resporption

227
Q

What are common manifestations of hypercalcemia?

A
  • Anorexia/Constipation
  • renal dysfunction (i.e., Nephrogenic diabetes insipidus, polydipsia)
  • MSK pain
228
Q

What are some signs for Immune Thrombocytopenia (ITP)?

A

Bruising
- Petechiae
- Ecchymoses
- Mucosal bleeding (i.e., Epitaxis, Heavy menses)

229
Q

What is the etiology of ITP?

A
  • Platelet autoantibodies
  • Preceding viral infection
230
Q

What are the laboratory findings for ITP?

A
  • Isolated thrombocytopenia (<100,000/mm3)
  • Few platelets (size normal to large) on peripheral smear
231
Q

What is the treatment for ITP?

A

Children:
- Observe if cutaneous symptoms only
- Glucocorticoids, IVIG, or anti-D if bleeding

Adults:
- Observation if cutaneous symptoms AND platelets >30,000/mm3
- Glucocorticoids, IVIG, or anti-D if bleeding or platelets <30,000/mm3

232
Q

What are some signs for Tumor Lysis Syndrome (TLS)?

A
  • Hyperuricemia: Purine nucleic acids are metabolized by xanthine oxidase to uric acid (often form obstructing uric acid stones in renal tubules - causing AKI)
  • Hyperphosphatemia: Tumor cells contain >3x more intracellular phosphate than healthy cells. Phosphate binds calcium in the renal tubules forming calcium-phosphate stones (causing AKI and systemic hypocalcemia)
  • Hyperkalemia: Can cause cardiac arrhythmias
233
Q

What are common manifestations of TLS?

A
  • Nausea
  • Vomiting
  • Myalgia
  • Fatigue
234
Q

What is the treatment approach for patients with TLS?

A
  • Aggressive IV Hydration
  • Uric acid reduction (i.e., rasburicase, allopurinol)
  • Treatment of electrolyte abnormalities
235
Q

What is the pathogenesis of Classic Congenital Adrenal Hyperplasia?

A
  • Autosomal recessive
  • 21 - Hydroxylase Deficiency (causing decreased cortisol and aldosterone and Increased 17-hydroxyprogesterone)

12-OHP is converted to testosterone leading to virilization (i.e., clitoromegaly/underdeveloped phallus, nonpalpable gonads) in genotypically female (46,XX)

236
Q

What is the clinical presentation of Classic Congenital Adrenal Hyperplasia?

A
  • Ambiguous genitalia in girls
  • Salt wasting syndrome:
    • Affects most girls and boys
    • Hypotension, dehydration, & Vomiting
237
Q

What are the laboratory findings for Classic Congenital Adrenal Hyperplasia?

A

Decreased Sodium and Glucose
Increased Potassium, and 17-hydroxyprogesterone

238
Q

What is the treatment for Classic Congenital Adrenal Hyperplasia?

A
  • Glucocorticoids & mineralocorticoids
  • High-salt diet
  • Psychosocial support
239
Q

What are some medications that cause hyperkalemia?

A
  • ACE inhibitors, ARBs
  • Cyclosporine
  • Digitalis
  • Heparin
  • Nonselective B-adrenergic blocker
  • NSAID
  • Potassium-Sparing Diuretic
  • Succinylcholine
  • Trimethoprim
240
Q

How do ACE inhibitors and ARBs cause hyperkalemia?

A

Decrease aldosterone section

241
Q

How do cyclosporines cause hyperkalemia?

A

Blocks aldosterone activity

242
Q

How do Digitalis medications cause hyperkalemia?

A

Inhibits Na/K-ATPase

243
Q

How does Heparin cause hyperkalemia?

A

Blocks aldosterone production

244
Q

How do non-selective B-adrenergic blockers cause hyperkalemia?

A

Interferes with B2-mediated intracellular potassium uptake

245
Q

How do NSAIDs cause Hyperkalemia?

A

Decreases renal perfusion –> decreased potassium delivery to the collecting ducts

246
Q

How does potassium sparring diuretics cause hyperkalemia?

A

Inhibits Epithelial Sodium channel (ENaC) or Aldosterone receptor

247
Q

How does Succinylcholine cause hyperkalemia?

A

Causes extracellular leakage of potassium through acetylcholine receptors

248
Q

How does Trimethoprim cause hyperkalemia?

A

Inhibits epithelial sodium channel

249
Q

What is Virchow’s Triad?

A
  • Hemostasis
  • Trauma (Endothelial Damage)
  • Hypercoagulability

Classic risk factors for venous stasis (i.e., DVT)

250
Q

What is Beck’s Triad?

A
  • diagnosis of acute cardiac tamponade
  • Jugular Venous Distention
  • Hypotension
  • Distant heart sounds
251
Q

What is an Aortic Aneurysm?

A

Defined: >50% dilatation of all 3 layers of the aortic wall

  • associated with atherosclerosis
  • Most are abdominal; >90% originate below renal arteries
252
Q

What is an Aortic Dissection?

A

Tear in the intima of a vessel; causing blood to enter the media - creating a false lumen

  • this leads to a hematoma, which propagates
  • Most commonly: secondary to hypertension
253
Q

Where is the most common site and age for Aortic dissection?

A
  • Above the aortic valve, distal to the left subclavian artery
  • 40-60 year olds; more male than female
254
Q

What is the treatment for Aortic Dissection?

A
  • Monitor and medically manage Blood pressure & Heart Rate
  • Begin B-blockade before starting vasodilators to prevent reflex tachycardia
  • Avoid thrombolytics
255
Q

Which type of aortic dissection is a surgical emergency?

A

Ascending aortic dissections

256
Q

What is the treatment for a DVT?

A
  • Anticoagulate with IV unfractionated heparin or SubQ Low-Molecular-weight-Heparin (LMWH) followed by PO warfarin for 3-6 months
  • Those with contraindications for anticoagulation:
    • IVC filters should be placed
  • Hospitalized patients should receive DVT prophylaxis:
    • exercise as tolerated
    • anti-thromboembolic stockings
    • SubQ unfractionated heparin or LMWH
257
Q

What the 6 P’s of acute ischemia?

A
  • Pain
  • Pallor
  • Paralysis
  • Pulse deficit
  • Paresthesias
  • Poikilothermia (inability to maintain a constant core temperature independent of ambient temperature)

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