UW 1 Flashcards

1
Q

ECG effects of Hyperkalemia

A

K: 6-7
PR prolongation
Tall t wave

K: 7-8
Flattening of P wave
ST segment elevation

K: >8
Widened QRS
AV Node block
Sine waves

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2
Q

Treatment of Hyperkalemia

A

C BIG K

Calcium chloride or gluconate (IV)
Bicarbonate, B-2 agonists
Insuline/Glucose
Kayexalate

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3
Q

Hypernatremia correction/management

A
  1. Determine free water deficit: total body water + (Na/140 -1)
  2. Rate of replacement: 0.5mEqL/L/H (over 48 to 72hrs)

Use normal saline until euvolemic

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4
Q

Hypernatremia Dxx

A

Urine Osmolality <300:
Diabetes insipidus

Urine Osmalality >600:
External losses (vomiting, diarrhea)
Na gain: hypertonic saline

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5
Q

Hyponatremia dxx

A

Look for algorithm pg 505 First aid step 2

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6
Q

Management of hyponatremia

A

Hypervolemic: loop diuretics

Euvolemia: Fluid restriction (1l/day) +/- diuretics. High Na diet

Hypovolemia: Saline

Correct over 72hrs (8-10 mEq/L/d) @ 0.5 mEq/L/h

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7
Q

K regulation

What cuases shif to intra or extracelluar space

A

Shift to intracellular space:
Insuline
B2 agonist
Alkalosis

Shift to extracellular space:
   Acidosis
   Increase osmolality
   Exercise
   Cell lysis
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8
Q

ECG findings in Hypokalemia

A

T wave flattening
U wave (additional wave after Twave)
ST segment depresion leading to AV block

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9
Q

Management of Hypokalemia

A
K repletion (oral preferred over IV)
If IV necessary: continuous infusion over bolus (do not exceed 20mEq/l/h
Bolus for symptomatic and ECG changes 
Replace magnesium (hypomagnesemia makes it difficult to correct K)
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10
Q

Hypercalcemia symptoms

A

Bones, stone, Groans, Psychiatric overtones;

Osteopenia/fractures
Kidney stones
Abdominal pain: anorexia constipation
Psychiatric overtones: weakness, fatigue, irritability, altered mental status

ECG: Short QT

Nephrogenic diabetes insipidus: Cant concentrate urine. May lead to dehidration

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11
Q

Hypocalcemia symptoms

A

Abdominal and muscle cramps
Dyspena
tetany
perioral and achral paresthesias

Chevostek sing (face twitch in facial stimulation)
Trousseau (arm spasm on pressure cuff)
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12
Q

Low Mg effect in Calcium regulation

A

Low Mg causes PTH resistance

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13
Q

Low Mg effect on electrolites

A

Low MG causes

Hypocalcemia
Hypokalemia

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14
Q

Defects in Renal Tubular Acidosis

A

Type I: H secretion
Type II: HCO3 reabsorption
Type III: Aldosterone resitance or deficiency

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15
Q

Why do you find sypmtoms of hypocalcemia in hyperventilating patients?

A

Hyperventilation causes Respitarory alkalosis
High pH cuases ionized Ca to bind to albumin because hydrogens ions are displaced
Total calcium is normal, ionized calcium decreases

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16
Q

AKI definition

A

Decline in renal function compared to a previous state in < 3months. (Increase in creatinine)

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17
Q

CKD definition

A

> 3months of GFR <60ml/min or sings of chronic kidney damage even with normal GFR

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18
Q

2 hyperparathyroidsm in CKD

A

Decreased phosphate excretion
decreased vitamin D production
Leading to hypocalcemia and renal osteodystrophy

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19
Q

Consequeances of renal failure

MAD HUNGER

A
Metabolic Acidosis
Dyslipidemia (especially triglerides)
Hyperkalemia
Uremia
Na/water retention
Growth retardation/development
Erithropoyetin failure
Renal osteodystrophy
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20
Q

Pathophysiology of AKI (types)

A

Prerenal: decreased perfusion
Intrinsic: injury within the nephron
Extrinsic: outflow obstruction

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21
Q

Labs in Prerenal vs Intrinsic AKI

A

BUN/Creatinine:
>20;1 (prerenal) <15:1(intrinsic)

FeNa and Urine Na
<1% <20mEq/L(prerenal) >2%>40mEq/L(intrinsic)

Urine Osmol
>500 (prerenal)
<350 (Intrinsic) damage tubules cant reabsorb
water, cant concentrate urine

Cast
Prerenal: Hyaline (more than normal) Intrinsic: RBC cast

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22
Q

Cuases of Acute interstital nephritis and Acute tubular necrosis

A

AKI after medication

Pee (diuretis)
Pain (NSAIDs)
Penicillins and cephalosporins
PPI
rifamPin

Acute tubular necrosis: ischemia, glomerulonephritis, rhabdomyolisis, embolic disease

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23
Q

Treatment of abnormal bleeding in uremia

A

Desmopressin

Increases factor VIII
Deficient in renal failure

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24
Q

AEIOU criteria of dialysis

A
Acidosis
Electrolite abnormalities
Ingestion (salicilates, theophyline, methanol, barbiturates, lithium, ethylene glycol)
Overload (fluids)
Uremia
25
Q

Labs in Rhabdomyolisis

A

High K and PO4. (due to cell lysis)
Low Ca due to deposition in damage tissue
CK >1000
Dark Urine with +blood test but no RBC

26
Q

Causes of rhabdomyolisis

A

Crush injury
Prolonged inmoblization (CNS depresants like opioids, benzos, alcohol)
Muscle activity (seizures and exercise)
Drug (statin, fibrates, colchicine, ethanol, cocaine)
Vasoconstriction: cocaine and amphetamines

27
Q

Pathophysiology of AKI in rhambdomyolisis (2)

A

Decreased renal perfusion (fluids toward damage tissue)

Direct damage from pigments

28
Q

VIPoma presentation

A

WDHA
Watery diarrhea
Hypokalemia
Achloridia

(Dehidration, muscle weakness, flushing)

29
Q

Exenatide: brand name, MOA, SE

A
  • exanatide = Byetta
  • MOA: GLP-1 receptor agonist
  • 2nd line w/metformin
  • low hypoglycemia risk
  • SE: weight loss
30
Q

Most common causes of folic acid deficiency

A
  • poor diet

- drugs: phenytoin, methotrexate, TMP

31
Q

Treatment for alcohol cravings (2)

A

Naltrexone (blocks u-opiod receptor blocker). Can precipitate opioid withdrawal in patients taking opioids.

Acamprostate: first line in patients with liver disease or opioid use. (MOA: glatamete modulator)

32
Q

Buprenorphine

A

Opioid partial agonist used in the treament of opioid use and pain management

33
Q

Smoking cessation pharmacologic treatment

A

Bupropion

Verenicline

34
Q

Acute dystonia treatment

A

Acute muscle contractions or spasm

Benztropine or dephinedramine

35
Q

Akathisia treatment

A

Perception of restlesness

B-blocker (propranolol)
Benzos and anticholinergics may work

36
Q

Parkinsonism treatment

A

Benztropine or amantadine

37
Q

Tardive dyskinesia managment (3)

A
  1. Stop agent or reduced dose if possible
  2. Valvenezine, deutetravenazine
  3. Switch to quetiapine or clozapine
38
Q

Indications for cystoscopy (6)

A
  1. Gross hematuria with no evidence of glomerular disease.
  2. Microscopic hematuria with no evidence of glomerular disease and high risk factors (smoking, chronic cistitys, paint, metal exposure; cyclophosphamide)
  3. Recurrent UTIs
  4. Obstructive symptoms with suspicious for stricture, stone
  5. Abnormal bladder imaging or cytology
  6. Irritative symptoms without infection
39
Q

Management of IUFD and complication

A

<24 weeks
Dilatation and evacuation

> 24 weeks
Labor induction

Fetal retention can lead to CID

40
Q

Insidious loss of peripheral vision
Need of frequent lens changes
Mild headache
Impaired adaptation to darkness

A

Open angle glaucoma

41
Q

Open angle glaucoma

A
Insidious loss of peripheral vision
Need of frequent lens changes
Mild headache
Impaired adaptation to darkness
Cupping of the optic nerve
42
Q

Open angle glaucoma treatment

A

Latanoprost, bimatoprost (topical prostaglandin, increases drainage)

B-blockers (timolol, betaxolol) to decrease aqueous humor production (careful in patients with asthma)

Pilocarpine to increase aqueous outflow
Acetazolamide (not as usefull in open angle)
Laser if medication fails

43
Q

Extreme sudden onset eye pain, blurred vision, headache, nausea and vomiting
Hard red eye, pupils dilated and non reactive

A

Closed angle glaucoma

44
Q

Closed angle glaucoma

A

Extreme sudden onset eye pain, blurred vision, headache, nausea and vomiting
Hard red eye, pupils dilated and non reactive

45
Q

Closed angle glaucoma treatment

A

B-blockers (timolol, betaxolol) to decrease aqueous humor production
Pilocarpine to increase aqueous outflow (cholinomimetic)
Acetazolamide
Laser if medication fails

46
Q

Test for corneal examination

A

Fluorescein exam

47
Q

Symptoms and Xray of pulmonary contusion

A

Tachypnea, tacycardia, hypoxia

Xray: 1st can be normal

Hours later:
Patchy pulmonary infiltrate (non restricted by
anatomic landmarks)

48
Q

Pes Anserious pain syndrome

A

Pain of medial aspect of knee below the joint line

Pes anserious is formed by: sartorious, semitendinous and gracilis tendon

Cause by over use or trauma, exacerbated by pressure of opposite knee when laying in the side

49
Q

Treatment for ADHD

A

Stimulants: amphetamines (metylphenidate, dextroamphetamine)

Non stimulant: atomoxetine

Others:
a2-adrenergics: clonidine, guanfacine
antidepresants: bupropione, TCAs

50
Q

Diseases associated with celiac disease

A

Down Syndrome

Other autoinmune: diabetis type 1, thyroiditis,

51
Q

Clinical sings suspecious for celiac disease in children /adolescents

A
Growth delay
Abdominal bloating / diarrhea
Microcitic anemia (sugesting nutritional deficiencies)
52
Q

Anti tissue transglutaminase antibody

A

Celiac disease

53
Q

REM behavior disorder

A

Motor behavior during REM
Dream enactment
Patient easily awaken and oriented
May be prodrome to Alpha-synuclein neurodegenerative disorders (parkinson, lewi body dementia, multiple system atrophy)

54
Q

Alpha-synuclein neurodegenerative disorders

A

Parkinson
Lewi body dementia (visual hallucinations, parkinsonism, fluctuation of consciousness)
Multiple system atrophy (parkinsonism, autonomic dysfuntion, wide spread neurological sings)

55
Q

Female patient with rapidly progressive shortness of breath, constipation, vomiting, abdominal distention. Palpable adnexal mass, not movil, nodular. Dx and managment

A

Possible Epithelial ovarian cancer
CA-125
Exploratory laparotomy. Hysterectomy/BSO with omectomy and paraaortic lymphadenopathy

56
Q

Painless Ulcer with raised borders Dxx

A

Syphilis: regional adenopathies. size 1-2cm

Granuloma inguinale: no adenopathies. Size 5-10mm

57
Q

Takayasu Arteritis

Presentation, Labs, Studies, Tx

A

Young asian female

Arm claudication, BP discrepancies between arms, pulse deficit (lower legs)

Constitutional symptoms

Elevated ESR, CRP
Thickening of vascular wall, narrowing of lumen
Aortic dilatation, widened mediastinum

Treat with systemic glucorticoid

58
Q

Management of solid brain metastasis

A

Surgery if stable extracraneal disease and good performance status