Critical Care Flashcards

1
Q

What are the characteristics of renal pain?

A
  • CC: colicky right-sided flank pain, nausea, vomiting, hematuria, CVA tenderness
  • Workup: UA, BUN/Cr, CT abdomen, renal US, KUB, blood cultures
  • Ddx: nephrolithiasis, renal cell carcinoma, pyelonephritis, GI etiology, glomerulonephritis, splenic rupture
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2
Q

What are the characteristics of pancreas pain?

A
  • CC: dull epigastric pain that radiates to the back
  • Workup: CT abdomen, CBC, electrolytes, amylase, lipase, AST, ALT, bilirubin, alkaline phosphatase, U/S abdomen
  • Ddx: pancreatitis, pancreatic cancer, peptic ulcer disease, cholecystitis/choledocholithiasis
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3
Q

What are the characteristics of gallbladder pain?

A
  • CC: RUQ pain
  • Workup: RUQUS, CBC, CMP, HIDA scan, MRCP/ERCP, amylase, lipase, alkaline phosphatase, bilirubin
  • Ddx: cholecystitis, choledocholithiasis, hepatitis, ascending cholangitis, Fitz-Hugh-Curtis syndrome, acute sub hepatic appendicitis
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4
Q

What are the characteristics of liver pain?

A
  • CC: RUQ pain, fever, anorexia, nausea, vomiting, dark urine, clay stool
  • Workup: CBC, amylase, lipase, liver enzymes, viral hepatitis serologies, UA, U/S abdomen, ERCP, MRCP
  • Ddx: acute hepatitis, acute cholecystitis, ascending cholangitis, choledocholithiasis, pancreatitis, primary sclerosis cholangitis, primary biliary cirrhosis, glomerulonephritis
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5
Q

What are the characteristics of spleen pain?

A
  • CC: severe LUQ pain that radiates to left scapula w hx of infectious mono
  • Workup: CBC, CXR, CT/US of the abdomen
  • Ddx: splenic rupture, splenic infarct, kidney stone, rib fracture, pneumonia, perforated peptic ulcer
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6
Q

What are the characteristics of stomach pain?

A
  • CC: burning epigastric pain after meals
  • Workup: rectal exam (occult blood in stool), amylase, lipase, lactase, AST, ALT, bilirubin, alkaline phosphatase, upper endoscopy (H. pylori biopsie), upper GI series
  • Ddx: peptic ulcer disease, perforated peptic ulcer disease, gastritis, GERD, cholecystitis, mesenteric ischemia, chronic pancreatitis
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7
Q

What are the characteristics of pipes pain?

A
  • CC: cramps abdominal pain, vomiting, abdominal distention, inability to pass flatus
  • Workup: rectal exam, CBC, electrolytes, CT abdomen/pelvis, colonoscopy
  • Ddx: intestinal obstruction, small bowel/colon cancer, volvulus, gastroenteritis, food poisoning, illness, hernia mesenteric ischemia/infarction, diverticulitis, with alternating diarrhea, constipation, diverticulitis, Crohn’s disease, ulcerative colitis, abscess, IBS, celiac disease, GI parasitic infection (amebiasis, giardiasis)
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8
Q

What are the characteristics of pelvis pain?

A
  • CC: RLQ pain, nausea, vomiting, dysuria, hematuria
  • Workup: pelvic exam, urine hCG, doppler U/S, rectal exam, UA, CBC, CT abdomen, laparoscopy, chlamydia, and gonorrhea testing
  • Ddx: ovarian torsion, appendicitis, ectopic pregnancy, ruptured ovarian cyst, pelvic inflammatory disease, bowel infarction/perforation, endometriosis, vaginitis, cysts, pyelonephritis
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9
Q

What are the characteristics of primary (Addison’s disease)?

A

autoimmune, infectious, disease of adrenal gland = decrease in cortisol secretion

  • adren gland destruction causing lack of cortisol and aldosterone secretion (usually autoimmune)
  • autoimmune (70%), infectious (tuberculosis), vascular (thrombosis/hemorrhage), metastatic, medications (rifampin, barbiturates, phenytoin, ketoconazole)
  • dx: increased ATCH, decreased cortisol, decreased aldosterone
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10
Q

What are the characteristics of secondary adrenal insufficiency?

A

pituitary adenoma or discontinuation of steroid - pituitary failure

  • exogenous steroid use (most common); hypopituitarism
  • dx: decreased ACTH, decreased cortisol, normal aldosterone
  • adrenal crisis = acute adrenal insufficiency
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11
Q

How is adrenal insufficiency dx?

A
  • 8 am serum cortisol and plasma ACTH alone with ACTH stimulation test
  • high ACTH, low cortisol = primary
  • low ACTH, low cortisol = secondary
  • CRH stimulation test: differentiates between causes of adrenal insufficiency
  • primary/Addison’s (adrenal): high ACTH, low cortisol
  • secondary (pituitary): low ACTH, low cortisol
  • adrenal autoantibodies can be assessed; CXR for TB (CT of adrenals)
  • autoimmune: atrophied adrenals
  • TB/granulomas: enlarged adrenals + calcification
  • bilateral adrenal hyperplasia = genetic enzyme defect
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12
Q

What is the tx of adrenal insufficiency?

A
  • Addison’s cortisol replacement therapy + androgen replacement
  • glucocorticoid + mineralocorticoid = hydrocortisone = 1st line, fludrocortisone for primary Addison’s disease only
  • Secondary: cause = focus of treatment (pituitary adenoma resection, wean steroid therapy slowly)
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13
Q

What are the characteristics of an upper GI bleed?

A

bleeding that originates proximal to the ligament of Treitz

  • hematemesis: vomiting of blood or coffee-ground emesis
  • melena: black tarry stool
  • orthostatic hypertension, tachycardia, abdominal tenderness - causes include:
  • peptic ulcer: upper abdominal pain
  • esophageal ulcer: odynophagia, gastroesophageal reflux, dysphagia
  • Mallory-Weiss tear: emesis, retching, or coughing prior to hematemesis
  • Esophageal varies with hemorrhage or portal hypertension: jaundice, abdominal distention (ascites)
  • Malignancy (gastric cancer and right-sided colon cancer): dysphagia, early satiety, involuntary weight loss, cachexia
  • Severe erosive esophagitis: odynophagia (painful swallowing), dysphagia and retrosternal chest pain
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14
Q

What is the tx of an upper GI bleed?

A
  • supportive care: NPO, IV access, oxygen, IV fluids of isotonic crystalloid
  • transufse for hemodynamic instability despite fluis, Hgb < 9 in high-risk patients (elderly, CAD), Hgb < 7 in low-risk patients
  • Treat with IV PPI until confiramtion of cause of bleeding - treat the underlyin cause
  • surgery - duodenotomy or gastroduodenostomy, ligation of bleeding
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15
Q

What are the characteristics of lower GI bleed?

A
  • Hematochezia (BRBPR): the passage of maroon or right red blood or clots per rectum
  • orthostatic hypotension or shock - causes include:
  • hemorrhoids: painless bleeding with wiping
  • anal fissures: severe rectal pain with defecation
  • proctitis: rectal bleeding and abdominal pain
  • polyps: painless rectal bleeding, no red flag signs
  • colorectal cancer: painless rectal bleeding and a change in bowel habits in a patient 50-80 years of age
  • diverticulosis is generally an incidental finding since diverticular bleeding is usually of greater volume
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16
Q

What is acute glaucoma?

A

increased IOP with optic nerve damage; an impediment to the flow of aqueous humor through trabecular meshwork; canal of Schlemm’s with increasing pressure in the anterior chamber
-open-angle = more common = > 40 yo, African Americans + family history

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17
Q

What is acute angle-closure glaucoma?

A

ophthalmic emergency - complete closure of the angle

  • classic triad: injected conjunctiva, steamy cornea, and fixed dilated pupil
  • painful eye/loss of vision, tearing, nausea, vomiting, diaphoresis
  • IOP acutely elevated
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18
Q

What is the tx of acute angle-closure glaucoma?

A

immediately refer to ophthalmology - start IV carbonic anhydrase inhibitor (acetazolamide), topical b-blocker (timolol), osmotic diuresis; laser/surgical iridotomy
-mydriatics (to dilate pupils) should NOT BE ADMINISTERED

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19
Q

What is open-angle glaucoma?

A

chronic, asymptomatic, potentially blinding disease

  • increased IOP, defects in the peripheral visual field, increased cup to disc ratio
  • asymptomatic until late in the disease, loss of peripheral vision = main symptoms
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20
Q

How is open-angle glaucoma dx?

A

can have elevated IOP without optic disc damage or optic nerve damage without increased IOP

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21
Q

What is the tx of open-angle glaucoma?

A

should be referred to an ophthalmologist for close monitoring

  • prostaglandin analogs are the 1’st line (ex. latanoprost), beta-blocker (timolol), alpha-agonist, a carbonic anhydrase inhibitor to decrease production
  • laser or surgical treatment
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22
Q

What is acute respiratory syndrome?

A

a type of respiratory failure characterized by fluid collecting in the lungs depriving organs of oxygen

  • increased permeability of alveolar-capillary membranes = development of protein-rich pulmonary edema (non-cariogenic pulmonary edema)
  • ARDS can occur in those who are critically ill or who have significant injuries = sepsis (most common), severe trauma, aspiration of gastric contents, near-drowning
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23
Q

What are the characteristics of ARDS?

A

People with ARDS have severe shortness of breath and often are unable to breathe on their own without support from a ventilator

  • rapid onset of profound dyspnea occurring 12-24 hours after the precipitating event
  • tachypnea, pink frothy sputum, crackles
  • chest radiograph shows air bronchograms and bilaterally fluffy infiltrate
  • normal BNP, pulmonary wedge pressure, left ventricule function and echocardiogram
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24
Q

What is the tx of ARDS?

A

identifying and managing underlying precipitation and secondary conditions

  • tracheal intubation with the lowest level PEEP to maintain PaO2 > 60 mmHG or SaO2 > 90
  • ARDS is often fatal, the risk increases with age and severity of illness
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25
Q

What is angina pectoris?

A

chest pain or discomfort, heaviness, pressure, squeezing, tightness is increased with exertion or emotion

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26
Q

What is stable angina?

A

predictable, relieved by rest and/or nitroglycerine

  • stress test demonstrates reversible wall motion abnormalities/ST depression > 1 mm
  • angiography provides a definitive diagnosis
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27
Q

What is the tx of stable angina?

A
  • beta-blockers and nitroglycerin

- severe: angioplasty and bypass

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28
Q

What is unstable angina?

A

previously stable and predictable symptoms of angina that are now more frequent, increasing or present at rest

  • chronic angina - increasing in frequency, duration, or intensity of pain
  • new-onset angina - sever and worsening
  • angina at rest
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29
Q

What is the tx of unstable angina?

A
  • admit to the unit with continuous cardiac monitoring, establish IV access, O2
  • pain control with NTG and morphine
  • ASA, clopidogrel, beta-blockers (first line), LMWH
  • rapid electrolytes
  • if the patient responds to medical therapy - stress test to determine if catheterization/revascularization necessary
  • reduce risk factors: stop smoking, weight loss, treat DM/HTN
  • Heparin
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30
Q

What is prinzmetal variant angina?

A

coronary artery vasospasm causing transient ST-segment elevations, not associated with clot

  • look for a history of smoking (#1 risk factor) or cocaine abuse
  • EKG may show inverted U waves, ST-segment of T-wave abnormalities
  • preservation of exercise capacity
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31
Q

What is the tx of prinzmetal variant angina?

A
  • stress testing with myocardial perfusion imaging or coronary angiography
  • pharmacotharpy SL, topical or IV nitrates (initial)
  • antiplatelet, thrombolytics, stains, BB
  • once diagnosis made - CCB and long-acting nitrates used for long-term prophylaxis (amlodipine)
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32
Q

What is cardiac arrest?

A

a sudden loss of blood flow resulting from the failure of the heart to pump effectively

  • signs include a loss of consciousness and abnormal or absent breathing
  • some individuals may experience chest pain, shortness of breath, or nausea before cardiac arrest
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33
Q

What is the cause of cardiac arrest?

A

V-tach or V-fib causes 75% of episodes of cardiac arrest

  • 5 Hs: Hypoxia, hypovolemia, hyperkalemia/hypokalmeia, H+ (acidosis), hypothermia
  • 5 Ts: tamponade, tension pneumothorax, toxins, thromboembolism (PE), thrombosis (MI)
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34
Q

What is the tx of cardiac arrest?

A
  • treatment for cardiac arrest includes immediate cardiopulmonary resuscitation (CPR) and if shockable rhythm is present, defibrillation
  • among those who survive, targeted temperature management may improve outcomes
  • an implantable cardiac defibrillator may be placed to reduce the chance of death from recurrence
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35
Q

What are premature beats?

A
  • PVC: early wide bizarre QRS, no p wave seen
  • PAC: abnormally shaped P wave
  • PJC: narrow QRS complex, no p wave or inverted p wave
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36
Q

What is paroxysmal supraventricular tachycardia?

A

narrow, complex tachycardia, no discernible P waves

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37
Q

What is atrial fibrillation/flutter?

A
  • A-fib: irregularly irregular rhythm with disorganized and irregular atrial activations and an absence of P waves
  • A-flutter: regular, sawtooth pattern and narrow QRS complex
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38
Q

What is sick sinus syndrome?

A
  • Brady-tachy: Arrhythmia in which bradycardia alternates with tachycardia
  • sinus arrest: the prolonged absence of sinus node activity (present P waves) > 3 seconds
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39
Q

What is sinus arrhythmia?

A

normal, minimal variations in the SA node’s pacing rate in association with the phases of respiration
-heart rate frequently increases with inspiration, decreases with expiration

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40
Q

What are premature ventricular contractions (PVCs)?

A

early wide “bizarre” QRS, no p wave seen

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41
Q

What is ventricular tachycarida?

A

three or more consecutive VBPs, displaying a broad QRS complex tachyarrhythmia

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42
Q

What is ventricular fibrillation?

A

erratic rhythm with no discernible waves (P, QRS, or T waves)

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43
Q

What is torsades de pointes?

A

polymorphic ventricular tachycardia that appears to be twisting around a baseline

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44
Q

What is a first degree AV block?

A

the PR interval is longer than 0.2 seconds or one block on EKG

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45
Q

What is type I second degree (Wenckebach)?

A

progressive lengthening of PR interval then missed QRS complex

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46
Q

What is type II second degree (Mobitz)?

A

fixed PR interval with occasional dropped QRS complexes

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47
Q

What is a third degree AV block?

A

no association between P waves and QRS complex

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48
Q

What is a bundle branch block?

A
  • Left: R and R’ (upward bunny ears) in V4-V6

- Right: R and R’ (upward bunny ears) in V1-V3

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49
Q

What is cardiac failure?

A

most common causes include CAD, HTN, MI, DM - LV remodeling: dilation, thinning, mitral valve incompetence, RV remodeling

  • exertional dyspnea (SOB), then with rest
  • chronic nonproductive cough, worse in a recumbent position
  • fatigue
  • orthopnea (late), night cough, relieved by sitting up or sleeping with additional pillows
  • paroxysmal nocturnal dyspnea
  • nocturia
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50
Q

What are the signs of cardiac failure?

A
  • Cheyne-Stokes breathing: periodic, cyclic respiration
  • Edema: ankles, pretibial (cardinal)
  • Rales (crackles)
  • S4 = diastolic HF (ejection fraction is usually normal)
  • S3 = systolic HF (reduced EF) with volume overload - tachycardia, tachypnea (rapid ventricular filling during early diastole is the mechanism responsible for the S3)
  • jugular venous pressure: > 8 cm
  • cold extremities, cyanosis
  • hepatomegaly ascites, jaundice, peripheral edema
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51
Q

What are the laboratories for heart failure?

A
  • CBC, CMP, U/A +/- glucose, lipids, TSH (occult hyperthyroidism or hypothyroidism)
  • Serum BNP: increases with age and renal impairment, low in obese, elevated in HF differentiates SOB in HF from non cardiac issues
  • 12-lead EKG
  • CXR: Kerley B lines
  • Echocardiogram (BEST TEST): diagnose, evaluate, manage most useful, differentiates HF +/- preserved LV diastolic function
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52
Q

What is New York Heart failure classification?

A
  • Class I (<5%) without any limitation of physical activity
  • Class II (10-15%) patients with slight limitation of physical activity, they are comfortable at rest
  • Class III (20-25%) patients with marked limitation of physical activity they are comfortable at rest
  • Class IV (35-40%) patients who are not only unable to carry on any physical activity without discomfort but who also have symptoms of heart failure or the anginal syndrome even at rest
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53
Q

What is the tx of systolic left heart failure?

A

Ace inhibitor + Beta blocker + loop

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54
Q

What is the tx for diastolic heart failure?

A

Ace inhibitor + beta blocker or CCB (do not use diuretics in stable chronic diastolic failure)

  • lasix - for diuresis
  • morphine - reduces preload
  • nitrates (NTG) - reduce preload O2
  • ACE inhibitor + diuretic (unless contraindicated)
  • CCB in diastolic HF
  • poor prognosis factors: chronic kidney disease, diabetes, lower LVEF, severe symptoms, old age
  • 5-y mortality: 50%
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55
Q

What is cardiac tamponade?

A

a buildup of fluid between the pericardial sac and the heart; constricts the heart
-heart unable to pump normally - blood flow through chambers obstructed - cardiac output decreases - hypotension - lower tissue perfusion - heart rate increases

56
Q

What are the causes of cardiac tamponade?

A
  • acute onset: trauma, myocardial infarction, aortic dissection, pericardial effusion
  • slow onset: cancer, chronic inflammation, uremic pericarditis, hypothyroidism, connective tissue disease
57
Q

What are the 3 D’s of cardiac tamponade?

A
Distant heart sounds
Distended jugular veins
Decreased arterial pressure = Beck's triad 
1. Hypotension 
2. Muffled heart sounds
3. Elevated neck veins (JVD)
58
Q

What is a classic finding of cardiac tamponade?

A

pulses paradoxus is a classic finding (drop 10 mmHg in systolic pressure on inspiration), narrow pulse pressure

  • EKG will show electrical alternans (while consecutive, normally-conducted QRS complexes alternate in height) and low voltage QRS complex
  • Chest x-ray finding - water-bottle heart (heart-shaped like a canteen)
  • treatment: pericardiocentesis
59
Q

What is coma?

A

a deep state of prolonged unconsciousness in which a person cannot be awakened

  • fails to respond normally to painful stimuli, light, or sound
  • lacks a normal wake-sleep cycle, and does not initiate voluntary actions
  • causes: structural brain lesiosn (bilateral), global brain dysfunction (metabolic or systemic disorders), psychiatric causes (conversion disorders, malingering)
60
Q

What are the initial steps of coma?

A
  • vitals, ABCs
  • assume underlying trauma (stabilize cervical spine) and assess for signs of underlying trauma
  • assess the level of consciousness using the Glasgow Coma Scale, repeat serially
61
Q

What are the brainstem reflexes?

A
  • pupillary light reflex - should be rounded, symmetrical and reactive to light
  • if responsive, midbrain intact
  • anisocoria (asymmetric pupils) - may be a sing of uncle herniation
  • pinpoint pupils - narcotics (morphine), ICH
  • bilateral fixed dilated pupils - severe anoxia
  • unilateral fixed, dilated pupil - CN 3 compression
  • eye movements - if cervical spine uninjured, perform an oculocephalic test (“dolls eyes”)
  • when head turned to one side, the eyes should move conjugately to the opposite direction if brainstem intake
  • if breathing on own, the brainstem is functioning
62
Q

How is coma dx?

A
  • labs - CBC, electrolytes, calcium, BUN, creatinine, glucose, plasma osmolatiry, ABG, EKG
  • toxicologic analysis of blood and urine
  • CT or MRI of brain
  • LP - if meningitis or SAH suspected
63
Q

What is the tx of coma?

A
  • correct reversible causes, treat the underlying cause
  • supplemental O2
  • naloxone for narcotic overdose
  • dextrose for hypoglycemia, thiamine before glucose load
  • correct electrolyte abnormalities
  • treat herniation - lower ICP
64
Q

What is diabetic ketoacidosis (DKA)?

A

is a medical emergency and complication of diabetes

  • patients have increased insulin requirements, which leads to a shortage, as a response the body begins burning excess fat (and fatty acids) causing ketone body accumulation
  • usually younger patients with type 1 DM
  • insulin deficiency = hyperglycemia = dehydration = ketonemia (anion gap metabolic acidosis) = potassium deficit
  • s/sx: thirst, polyuria, polydipsia, nocturia, weakness, fatigue, confusion, n/v, fatigue, chest pain, abdominal pain
  • PE: tachycardia, tachypnea, hypotension, decreased skin turgor, fruity breath/Kussmaul’s respiration
65
Q

How is diabetic ketoacidosis dx?

A

lab values seen in DKA include blood sugars above 250 mg/dL and anion gap metabolic acidosis with pH below 7.3 and bicarbonate below 18

  • patients will also show preset plasma ketones
  • due to an extracellular shift, patients may be hyperkalemic
66
Q

What are the lab values of mild DKA?

A
plasma gluocse > 250
arterial pH >7.3
serum bicarb 15-18
ketones positive
serum osm variable
67
Q

What are the lab values of moderate DKA?

A
plasma gluocse > 250
arterial pH 7 -7.24
serum bicarb 10-<15
ketones positive
serum osm variable
68
Q

What are the lab values of severe DKA?

A
plasma gluocse > 250
arterial pH <7
serum bicarb <10
ketones positive
serum osm variable
69
Q

What is the tx of DKA?

A

IV fluids = critical 1st step!!
-regular insulin (lowers serum glucose and switches the body from catabolic to anabolic state); potassium, bicarb in severe acidosis

70
Q

What is fasting hypoglycemia?

A
  • consider insulinomas in healthy patients with fasting hypoglycemia
  • etiology: hypopituitarism, Addison disease, myxedema, acute alcoholism, liver failure, ESRD
  • MC: adenoma of islets of Langerhans (90% benign), rare)
  • confusion, blurred vision, diplopisa, anxiety, seizures
  • Dx:
  • serum glucose < 45 mg/dL
  • symptoms begin at plasma glucose levels < 60 mg/dL
  • impairment of brain function at 50 mg/dL
  • serum insulin, proinsulin, and C-peptide: inappropriately high sulfonylurea screening (-)
  • other labs: serum ketones, antibodies to insulin
  • plasma BOH <2.7 mmol/L
71
Q

What is the tx for fating hypoglycemia?

A
  • home glucose monitor
  • measure the time of symptoms and prior consumption of carbs
  • if high clinical suspicion despite an outpatient trial
  • 62 h supervised inpatient fast
  • surgical resection of insulin-secreting tumors
72
Q

What is medication-induced hypoglycemia?

A

common offenders: FQ, quinine, ACE inhibitors, salicylates, beta-blocker

73
Q

What is the tx of medication-induced hyoglycemia?

A

glucose administration to replenish glycogen stores until gluconeogenesis resumes

74
Q

What is factitious hypoglycemia?

A
  • self-induced hypoglycemia
  • patient has access to insulin or sulfonylureas taken by another family member; hypoglycemia
  • immunoreactive insulin: elevated; low plasma C peptide, insulin, C-peptide ratio > 1
75
Q

What is postprandial hypoglycemia?

A
  • causes: s/p gastric surgery (gastrectomy, vagotomy, pyloroplasty, Nissen fundoplication, etc)
  • sx occur after eating high carb meal; lightheadedness, sweating, confusion, loss of consciousness, anxiety
  • signs: palpitations, diaphoresis
76
Q

What is the tx of postprandial hypoglycemia?

A
  • dietary modification
  • smaller meals of less rapidly digested carbs
  • reduced intake of refined sugars
  • increased dietary fiber intake
  • Octreotide 50 ug SQ 2-3 times/day, 30 min prior to meals
77
Q

What is insulin-induced hypoglycemia?

A
  • patient should carry glucose tablets or juice at all times
  • ingestion of 15 g of carbs in most cases
  • check glucose in 15 min and treat again if still low
  • IM 1 mg glucagon emergency kit
  • inject AQ/IM into buttock, arm, or thigh
  • turn patient on side to prevent aspiration of vomit
  • for sever hypoglycemia 50 mL, D5W rapid IV infusion or 1 mg IM glucagon
78
Q

What is hypertensice emergency?

A

BP usually > 180/120 WITH impending or progressive end-organ damage

79
Q

What is hypertensive urgency?

A

BP usually > 180/120 WITHOUT signs of end-organ damage

80
Q

What is malignat HTN?

A

diastolic reading >140 associated with papilledema and either encephalopathy or nephropathy

81
Q

What is the tx for hypertensive emergency?

A

sodium nitroprusside (drug of choice)

82
Q

What is the tx for hypertensice urgency?

A

clonidine (drug of choice)

83
Q

What is the tx for malignant hypertension?

A

hydralazine

84
Q

What is a non-ST segment elevation MI?

A

(NSTEMI, subendocardial MI) is myocardial necrosis (evidenced by cardiac markers in the blood; troponin I or troponin T and CK will be elevated) WITHOUT acute ST-segment elevation or Q waves

  • ECG changes such as ST-segment depression, T-wave inversion, or both may be present (without elections)
  • coronary artery not completely blocked
  • subendocardial infarct
85
Q

What are the sx of NSTEMI?

A

chest pain with shortness of breath, with possible radiation to the neck, jaw, arms, shoulders, and back

86
Q

How is a NSTEMI dx?

A

the typical workup includes

  • EKG
  • Troponin I
  • BNP
  • CXR
  • CBC/CMP
87
Q

What cardiac markers will be elevated?

A
  • troponin is most sensitive and specific appears at 2-4 hours, peaks 12-24 hours and lasts for 7-10 days
  • CK/CK-MB appears at 4-6 hours, peaks at 12-24 hours and returns to normal within 48-72 hours
  • myoglobin (Mb) is used less than the other markers and appears at 1-4 hours, the peak is 12 hours, and returns to baseline levels within 24 hours
88
Q

How is a NSTEMI tx?

A

beta blockers + NTG + aspirin and clopidogrel + heparin + ACEI + statins + reperfusion

  • reperfusion via percutaneous coronary intervention (not thrombolysis)
  • less time-sensitive than in STEMI
89
Q

What is a STEMI?

A

is myocardial necrosis (evidenced by cardiac markers in the blood, troponin I or troponim T and CK will be elevated) WITH acute ST-segment elevation or Q waves

  • coronary artery completely blockers; full thickness of myocardial wall involved
  • ECG shows ST elevation, possible Q waves
90
Q

What are the sx of STEMI?

A

chest pain with shortness of breath, with possible radiation to the neck, jaw, arms, shoulders, and back

91
Q

How is a STEMI dx?

A

the typical workup includes

  • EKG
  • troponin I
  • BNP
  • CXR
  • CBC/CMP
92
Q

What are the EKG findings related to the location of infarction?

A
  • anterior wall infarction: Q waves and ST elevation in leads I, AVL, and V2 to V6
  • inferior wall infarction: Q waves and ST elevation in leads II, III and AVF
  • lateral wall infarction: ST elevation in the lateral leads (I, aVL, V5-6), reciprocal ST depression in the inferior leads (III and aVF)
  • posterior wall infarction: ST depressions in V1 to V3
93
Q

What is the tx for STEMI?

A

Beta blcokers + NTG + aspirin and clopidogrel + heparin + ACEI + statins + reperfusion

  • aspirin and clopidogrel are given at once
  • very time sensitive - immediate (within 90 minutes) coronary angiography and pricamary PCl
  • thrombolytic therapy within the first 3 hours if PCI not available
94
Q

What are the absolute contraindications for fibrinolytic use in STEMI include the following?

A
  • prior intracranial hemorrhage (ICH)
  • known structural cerebral vascular lesion
  • known malignant intracranial neoplasm
  • ischemic stroke within 3 months
  • suspected aortic dissection
  • active bleeding or bleeding diathesis (excluding menses)
95
Q

What is a pericardial effusion?

A

excess fluid between the heart and pericardium
-abnormal accumulation of inflammatory fluid, immune cells - diffuse into interstitial - fluid pools in pericardial space - pericardial dilation - pressure or heart, vena cava - decreased cardiac filling - cardiac tamponade - decreased cardiac output

96
Q

What are the causes of pericardial effusion?

A

aortic dissection, heart failure, hypoalbuminemia, lymphatic obstruction, malignancy, radiation, renal failure, trauma, autoimmune disease, acute pericarditis (viral, bacterial, tuberculosis, idiopathic in origin), myxedema, some drugs, iatrogenic, idiopathic

  • same symptoms as acute pericarditis expect patients will now have signs of fluid buildup around the heart which include low voltage QRS complexes, electrical alternans, distant heart sounds and an echocardiogram showing a collection of pericardial fluid
  • EKG showing low voltage QRS along with electrical alternans
  • echocardiogram with increased pericardial fluid
  • radiograph: water bottle heart
97
Q

What is the tx of pericardial effusion?

A

underlying cause, pericardiocentesis if the effusion is large
-electrical alternans as seen by changing QRS amplitudes best seen in lead II

98
Q

What is a pneumothorax?

A

is a collapsed lung caused by an accumulation of air in pleural space
-presents with acute onset ipsilateral chest pain and dyspnea with decreased tactile remits, deviated teaches, hyperresonance, diminished breath sound

99
Q

What are the characterisic of pneumothorax?

A

can be spontaneous or traumatic

  • primary: occurs in absence of underlying disease (tall, thin males ages 10-30 at greatest risk)
  • secondary: in presence of underlying disease (COPD, asthma, cystic fibrosis, interstitial lung disease)
100
Q

What is a tension pneumothorax?

A

penetrating injury - air in pleural space increasing and unable to escape

  • a mediastinal shift to the contralateral side and impaired ventilation
  • CXR = pleural air; ABG shows hypoxemia
101
Q

What is the tx of pneumothorax?

A

treatment depends on the size

  • small - <15% diameter of hemithorax will resolve spontaneously without the need for chest tube placement
  • large - >15% diameter and symptomatic pneumothoraces require chest tube placement
  • serial CXR every 24 hours until resolved
  • tension pneumothorax is a medical emergency, large bore needles to allow air out of the chest, chest tube for decompression
102
Q

What is a pulmonary embolism?

A

a blockage in one of the pulmonary arteries in the lungs

  • more than 90% originate from clots in the deep veins of the lower extremities
  • presents with dyspnea (most common) and pleuritic chest pain)
  • R/F: Virchow’s triad = hyper-coagulable state, trauma, venostasis (surgery, cancer, oral contraceptives, pregnancy, smoking, long bone fractures/fat emboli)
  • Homan’s sign: (dorsiflexion of the foot causes pain in calf) indicative of deep vein thrombosis
  • EKG: tachycardia (most common), S1Q2T3 (rare), non-specific ST wave changes
103
Q

How is a pulmonary embolism dx?

A

Well’s score is used to assess the probability of pulmonary embolism

  • spiral CT = initial method of identifying
  • pulmonary angiography = gold standard definitive
  • CXR: Westermark sign or Hampton hump (triangular or rounded pleural base infiltrate adjacent to hilum)
  • VQ scnas are “old school” = perfusion defects with normal ventilation (normal VQ rules out PE; abnormal - non-specific)
  • venous duplex ultrasound of lower extremities (normal test does not exclude PE)
  • ABG = respiratory alkalosis secondary to hyperventilation
  • D-dimer
104
Q

What is the tx for pulmonary embolism?

A

heparin is the anticoagulant of choice for the acute phase with factor Xa inhibitors (eg, rivaroxaban, apixaban, edoxaban) and oral direct thrombin inhibitors (dagigatran) thereafter

  • warfarin for patients in whom factor Xa or direct thrombin inhibitors are not available and for patients with sever renal insufficiency (target INR range 2.0-3.0)
  • duration of treatment: minimum of anticoagulation 3 months with reversible risk factor
  • unprovoked: anticoagulation recommended for at least 6 months then reevaluate
  • two episodes unprovoked, long term with anticoagulation
105
Q

What is a focal seizures with retained awareness (consciousness maintained)?

A
  • this type of focal seizure was previously known as a simple partial seizure
  • no alteration in consciousness, abnormal movements or sensations
106
Q

What is a focal seizures with a loss of awareness (consciousness impaired)?

A
  • this type of focal seizure may also be called a focal dyscognitive seizure (previously known as complex partial seizures)
  • altered consciousness, automatisms (ie. lip-smacking)
  • presents with a postictal state (confusion and loss of memory) which differentiate them from absence seizures
107
Q

What is the tx of focal seizures?

A

phenytoin and carbamazepine are drugs of choice

108
Q

What is a generalized seizures?

A

occur when there is widespread seizure activity in the left and right hemispheres of the brain
-start midbrain or brainstem and spreads to both cortices

109
Q

What is an absence seizures?

A

(formerly known as petit Mal)
characterized by a brief impairment of consciousness with an abrupt beginning and ending
-at times involuntary movements may occur, but they are uncommon and the patient has no recollection and witnesses commonly miss them

110
Q

What is a tonic-clonic or convulsive seizures?

A

(formerly known as grand Mal)

  • bilaterally symmetric and without focal onset
  • begins with a sudden loss of consciousness - a fall to the ground
  • tonic phase: very stiff and rigid 10-60 seconds
  • clonic phase: generalized convulsions and limb jerking
  • postictal phase: a confused state
111
Q

What is an atonic seizure?

A

(also knowns as drop attacks)

-looks like syncope, sudden loss of muscle tone

112
Q

What is a clonic seizures?

A

during a clonic seizure, a person may lose control of bodily functions and begin jerking in various parts of the body
-he/she may temporarily lose consciousness, followed by confusion

113
Q

What is a tonic seizure?

A

extreme rigidity then immeidiate LOC, but not followed by a clinic phase

114
Q

What is a myoclonic seizures?

A

muscle jerking, but not the tonic phase, occurs in the morning

115
Q

What is a febrile seziure?

A

convulsion associated with an elevated temperature greater than 38, > 6 mos < 5 years, absence of central nervous system infection or inflammation

116
Q

What is an infantile spasms?

A

type of epilepsy seizure but they do not fit into the category of focal or generalized seizures

117
Q

What is psychogenic non-epileptic seizures (PNES)?

A

not due to epilepsy but may look very similar to an epilepsy seizure

118
Q

What is status epilepticus?

A

a single epileptic seizure lasting more than five minutes or two or more seizures within a five-minute period without the person returning to normal between them

  • two forms: convulsive and non convulsive
  • convulsive status epileptic presents with a regular pattern of contraction and extension of the arms and legs
  • nonconvulsive status epilepticus includes a complex partial status epilepticus and absence status epilepticus
119
Q

What is the tx of status epilepticus?

A

benzodiazepines (lorazepam) are the preferred initial treatment after which typically phenytoin is given

120
Q

What is shock?

A

is the state of insufficient blood flow to the tissues of the body as a result of problems with the circulatory system

  • symptoms include weakness, hypotension, tachycardia, tachypnea, sweating, anxiety, and increased thirst
  • malfunction of organ systems: lactic acidosis, renal (anuria/oliguria), CNS dysfunction (AMS)
121
Q

What is the tx of shock?

A

ABC assessment

  • initial steps: stabilie patient hemodynamically, determine the cause
  • fluid bolus (500-1000 L NS or lactated ringer’s solution)
  • CBC, CMP, Creatinine, PT/PTT, continuous pulse oximetry
  • EGK, CXR
  • vasopressors (dopamine or norepinephrine) if hypotensive despite IVF
122
Q

What is cardiogenic shock?

A
  • heart is unable to generate cardiac output
  • post-acute MI - cardiac tamponade, tension pneumothorax, arrhythmias, PE, CM, myocarditis, valvular defects
  • SBP < 90 urine output <20 mL/h altered sensorium, pale cool skin, hypotension, tachycardia, JVD pulmonary congestion
  • Dx: EKG: ST elevation (most common) echo hemodynamic monitoring
123
Q

What is the tx of cardiogenic shock?

A
  • ABCs
  • Identify underlying cause
  • vasopressors: Dopamine (initial) +/- dobutamine
  • NTG or nitroprusside
  • IVF - harmful if LV pressures elevated (may need diuretics)
124
Q

What is hypovolemic shock?

A

decreased circulatory blood volume - decreased preload and cardiac output

  • hemorrhage (trauma, GI bleed, retroperitoneal)
  • nonhemorrhagic - vomiting, diarrhea, dehydration, burns, third space loss
  • vital signs and clinical picture
  • Dx: central venous line or pulmonary artery catheter: decreased CVP/PCWP, decreased cardiac output and increased SVR
125
Q

What is the tx of hypovolemic shock?

A
  • AB: intubation, mech vent
  • circulation: direct pressure if acute bleed
  • IV hydration: class II (optional), class III/IV (required)
126
Q

What is neurogenic shock?

A
  • failure of sympathetic NS to maintain vascular tone
  • SCl, head injury, spinal anesthesia, drug blockade
  • dx: vasodilation with decreased SVR (warm, flush skin), UOP, NL to LOW, bradycardia, hypotension
127
Q

What is the tx of neurogenci shock?

A
  • judicious use of IV fluids
  • vasoconstrictors to restore venous tone
  • supine or trendelenburg position
  • maintain temp
128
Q

What is septic shock?

A
  • hypotension induced by sepsis, persistent despit adequate IVF - multi-organ system failure
  • pneumonia, pyelonephritis meningitis, abscess, cholangitis, cellulitis, peritonitis
  • severe decrease in SVR due to peripheral vasodilation (flush, warm skin)
  • signs of SIRS
  • signs of shock: hypotension, oliguria, lactic acidosis
  • fever or hypothermia
  • dx: decreased EF - reduced contractility; clinical DX: (+) blood cultures x 2 source of infection
  • tx: iv antibiotics (broad-specturm) at max doses
  • IVF:
  • increase mean BP
  • pressors: maintain BP
129
Q

What is status epilepticus?

A

a single epileptic seizure lasting more than five minutes or two or more seizures within a five-minute period without the person returning to normal between them

130
Q

What are the two forms of status epilepticus?

A

consulsive and nonconsulsive

  • convulsive status epilepticus presents with a regular pattern of contraction and extension of the arms and legs
  • nonconvulsive status epilepticus includes complex partial status epilepticus and absence status epilepticus
131
Q

What is the tx of status epilepticus?

A
  • place in left lateral decubitus position (suppressed gag reflex = prone to aspiration of gastric contents)
  • benzodiazepines (lorazepam) are the preferred initial treatment after which typically phenytoin is given
  • watchful waiting for auto-correction of acidosis once seizure activity is controlled
  • untreated generalized seizures lasting > 60 min may result in permanent brain damage; longer-lasting seizures may be fatal
132
Q

What is a thyroid storm?

A
  • thyroid storm is an acute form of hyperthyroidism that results from untreated or inadequately treated severe hyperthyroidism
  • it is rare, occurring in patients with Graves disease (MC) or toxic multinodular goiter
  • it may be precipitated by infection, trauma, surgery, embolism, diabetic ketoacidosis, or preeclampsia
133
Q

What are the s/sx of thyroid storm?

A

heat intolerance, palpitations, weight loss, tachycardia, anxierty, jaundice
-jaundice = hepatic tissue hypoxia due to increased peripheral consumption of oxygen

134
Q

What is the clinical presentation of thyroid storm?

A

tachycardia HR >140, heart failure, hypotension, dysrhythmia (fib), hyperpyrexia (104-106 F), agitation, psychosis, coma; hyperreflexia, goiter, exophthalmos, pretibial edema

135
Q

How is thyroid storm dx?

A

labs: free t4/t3, tsh - low tsh and high free T4

136
Q

What is the tx for thyroid strom?

A

beta-blocker, thionamides, iodine, hydrocortisone, bile ace sequestrants

  • propylthiouracil - inhibits the conversion of thyroxine to triiodothyronine
  • methimazole or PTU (PTU if pregnant)