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A+ Test Prep > #Acid&Base/Endocrine > Flashcards

#Acid&Base/Endocrine Flashcards

0
Q

pH & potassium change calculation

A

pH 0.1 = K 0.6 in opposite direction.

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1
Q

Describe how PaCO2 change will effect pH

A

PaCO2 change 10 mmHg = pH change 0.08

Opposite Direction.

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2
Q

PaCO2 & K change equation

A

PaCO2 10 torr = K 0.5 mEq/l (same direction)

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3
Q

To increase serum potassium 1 mEq/L, how much potassium must be given?

A

100-200 mEQs

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4
Q
  1. DKA: don’t drop glucose levels faster than:

2. At what bs do you start d5w?

A
  1. 100 mg/dL/hr

2. <300 mg/dL

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5
Q

Oat cell carcinoma: mimics which 2 hormones causing which 2 syndromes.

A
  • ADH: SIADH (no urinating)
  • cortisol : cushings disease (adrenal overloaed)

(Small cell carcinoma typically in lungs)

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6
Q

Causes of SIADH

A

(Syndrome of innappropriate Antidiuretic syndrome)

  • oat cell carcinoma
  • viral pneumonia & TB
  • head injury
  • opiates, pain, anxiety (temporary)
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7
Q

SIADH presentation

A 
Dilution army hyponatremia 
=cerebra edema
=seizures
=elevated urine osmolality / specific gravity
       -fluid doesn't get into kidneys
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8
Q

Treatment for SIADH

A
  • restrict fluids
  • Diuresis: 1st degree loop diuretics
  • demeclocycline (tetracycline fam / ADH receptor antagonist)
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9
Q

Thyroid storm aka, presentation, tx

A

Graves’ disease
Presentation: high idle speed, weight loss, cp, sob, fever, tremors/nervousness, marked tachycardia, AFib.

Tx: anti thyroid meds, antipyretics, electrolytes, fluids, glucocorticoids (dexamethasone= prevents production t4-t3), hr will not respond to digitalis.

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10
Q

Myxedema Coma cause, presentation, tx

A

Hypothyroidism - autoimmune due to infection
Presentation: women, >60, winter. Fatigue, weight gain, cold intolerance, deep voice, coarse hair. ALOC=coma

Tx: supportive, IV levothyroxine (t4), watch for adrenal insufficiency.

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11
Q

Steroid production pathway

Steroid mechanisms:

A

CRH (cortical releasing hormone) released from brain. > to anterior pituitary > release of ACTH (adrenal corticotropin hormone) > to adrenals > release of glucocorticoids, androgens, mineralcorticoids.

Management of sugars, breakdown from muscles, fatty tissues, sex hormones, electrolytes, aldosterone levels, alpha/beta receptor response.

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12
Q

Addison’s causes (primary/secondary)

A

Primary: autoimmune
Secondary: pituitary malfunction = low ACTH
Other: acute glucocorticoid withdraw

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13
Q

Addison’s presentation, tx

A

Presentation: inadequate aldosterone cortisol, androgens. Fatigue, weakness, low BP, low h2o / Na retention, hypoglycemia, poor catecholamine response.

Tx w/steroids, fluid

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14
Q

Cushings disease causes, presentation, tx

A

Causes: chronic steroid use w/ abrupt DC, pituitary disorder (high ACTH), oat cell, adrenal carcinoma (high cortisol)
Presentation: upper body obesity, thin arms/legs (muscle wasting), round face, buffalo hump, fatique, HTN, high BS, fatty & amino acids to glucose, pancreatic overload (DMII)’ increase Epi/NE
TX: steroid management, supportive, surgery.
Solu-cortef (low potency), Decadron high potency.

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15
Q

Pancreatitis causes

A

ETOH, biliary stone, steroids & antibiotics, viral/bacterial infection, bowel obstruction

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16
Q

Pancreatitis presentation (7)

A
  1. Low ca
  2. L base atelectasis = elevation L diaphragm
  3. Bilateral pleural effusion
  4. Sepsis & ARDS
  5. Renal failure
  6. Cullen’s sign: peri umbilical bruising
  7. Gray-Turner’s sign: flank & groin bruising
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17
Q

Pancreatitis tx (7)

A
  1. Fluid resuscitation
  2. NPO, NG/OG (stimulate stomach=stimulate pancreas)
  3. Meperidine (similar to atropine, increased GI motility / relaxation, sphincter if odi relaxation)
  4. Alternate atropine, Narcan, beta blockers, tetrodotoxin
  5. Anticipate progression (ARDS, Sepsis, MOzdS, DIC)
  6. Antibiotics for sepsis
  7. Surgery
18
Q

Why is liver failure common w/ GI bleeds?

A

Body is metabolizing blood proteins

-metabolism of proteins = ammonia production

19
Q

Liver failure / hepatic encephalopathy presentation

A

Elevated AST, ALT, SGOT/SPGT,
Elevated BUN (Ammonia coverts to blood urea nitrogen)
Hypokalemia - K follows ammonia as excreted

20
Q

Kehr’s sign

A

Splenic - L shoulder pain

21
Q

Brudzinski vs kernig sign

A

Brudzinski’s: flex neck, want to bring hamstring up
Kernig: brig up hamstring, want to flex neck.

(Releases tension on hamstrings)

22
Q

Murphy’s sign

A

Gall bladder - push on RUQ

  • traps gallbladder between hand n liver
  • pt cannot take a deep breath.
23
Q

Venous blood gasses

A 
PH 7.31-7.41
PvCO2 40-50
HCO3 22-26
PvO2 35-40
SvO2 70-75%
BE -2 to 2
24
Q

HCO3 change = pH change

A

HCO3 10 mEq = pH 0.15 (same direction)

25
Q

Bicarbonate replacement therapy

A

(Weight kg/4) x BE

1/2 given IVP
1/2 given in L fluid / hr

26
Q

Minute ventilation calculation & normal value

A

Ve = Vt x f (frequency)

Normal value: 6.0 LPM

27
Q

Alveolar minute ventilation calculation & normal value

A

Va = (Vt - Vd) x f

Vd=dead space (.33Vt or 1ml/lb IBW)

Normal: 4.2 l/min

28
Q

Attempting to blow off co2, adjust vent rate or volume?

A

Increase rate, decrease volume = decrease Va

Decrease rate, increase volume = increase Va

29
Q

Normal anion gap

A

8-16 (w/o K)

10-20 (w/ K+)

30
Q

4 primary suspects of metabolic acidosis

A

1: lactic Acidosis

  1. DKA
  2. Renal failure
  3. Toxins
31
Q

MUD PILES

A 
M - methanol
U - uremia
D - DKA
P - paraldehyde
I - isoniazide
L - lactate
E - Ethylene Glycol
S - Salicylate
32
Q

How quickly can magnesium be administered?

A

1g / 30 minutes (sometimes faster)

33
Q

Alveolar O2 pressure calculation

A

PAO2 = FiO2 (PBAR -PH2O) - 1.2 (PaCO2)

PBAR: barometric pressure
PH2O: waster pressure, constant (lung humidity: 100% =47 torr)

34
Q

Aa-Gradient calculation, normal, slight shunt, definite shunt values.

A

PAO2 (alveolar O2 pressure) - PaO2 (ABGs)

Norm: 5-20
Slight shunt: >10
Definite shunt: >20

35
Q

Steps to improve PaO2

A
  1. Assure adequate Va (Vt / rate)
  2. Maximize FiO2
  3. PEEP
  4. Invert I:E
36
Q

Which blood type patient is most likely to produce a hemolytic reaction?

A

Type O patient - can only receive type O blood

37
Q

What percentage of Hemolytic reactions will result in DIC?

A

30-50%

38
Q

Hemolytic reaction treatment

A
  • Support hemodynamics (fluids & pressors)
  • maintain renal perfusion (fluid & diuretics)
  • prevent DIC (maintaining pressure & oxygenation)
39
Q

Circulatory overload post blood administration cause

A

Blood is colloidal - draws fluid into vascular space

40
Q

Fresh frozen plasma primary indications

A
  • Coumadin therapy reversal
  • DIC
  • Antithrombin III deficiency (prolonged heparin therapy)
  • dilutional coagulopathy (>1 blood volume or 10 units PRBC)
  • volume expander
41
Q

FFP commonly given with PRBCs at what rate

A

1:4 with PRBCs until 10 units PRBCs in then 1:1.

42
Q

FFP dosage

A

Driven by coags (Pt/PTT) >1.5 - 1.8 x normal

43
Q

FFP and Coumadin

A

Coumadin interferes with vit K

-Vit K

A+ Test Prep (28 decks)

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