Flashcards in #Acid&Base/Endocrine Deck (44):
Describe how PaCO2 change will effect pH
PaCO2 change 10 mmHg = pH change 0.08
pH & potassium change calculation
pH 0.1 = K 0.6 in opposite direction.
PaCO2 & K change equation
PaCO2 10 torr = K 0.5 mEq/l (same direction)
To increase serum potassium 1 mEq/L, how much potassium must be given?
1. DKA: don't drop glucose levels faster than:
2. At what bs do you start d5w?
1. 100 mg/dL/hr
2. <300 mg/dL
Oat cell carcinoma: mimics which 2 hormones causing which 2 syndromes.
-ADH: SIADH (no urinating)
-cortisol : cushings disease (adrenal overloaed)
(Small cell carcinoma typically in lungs)
Causes of SIADH
(Syndrome of innappropriate Antidiuretic syndrome)
-oat cell carcinoma
-viral pneumonia & TB
-opiates, pain, anxiety (temporary)
Dilution army hyponatremia
=elevated urine osmolality / specific gravity
-fluid doesn't get into kidneys
Treatment for SIADH
-Diuresis: 1st degree loop diuretics
-demeclocycline (tetracycline fam / ADH receptor antagonist)
Thyroid storm aka, presentation, tx
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.
Myxedema Coma cause, presentation, tx
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.
Steroid production pathway
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.
Addison's causes (primary/secondary)
Secondary: pituitary malfunction = low ACTH
Other: acute glucocorticoid withdraw
Addison's presentation, tx
Presentation: inadequate aldosterone cortisol, androgens. Fatigue, weakness, low BP, low h2o / Na retention, hypoglycemia, poor catecholamine response.
Tx w/steroids, fluid
Cushings disease causes, presentation, tx
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.
ETOH, biliary stone, steroids & antibiotics, viral/bacterial infection, bowel obstruction
Pancreatitis presentation (7)
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
Pancreatitis tx (7)
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
Why is liver failure common w/ GI bleeds?
Body is metabolizing blood proteins
-metabolism of proteins = ammonia production
Liver failure / hepatic encephalopathy presentation
Elevated AST, ALT, SGOT/SPGT,
Elevated BUN (Ammonia coverts to blood urea nitrogen)
Hypokalemia - K follows ammonia as excreted
Splenic - L shoulder pain
Brudzinski vs kernig sign
Brudzinski's: flex neck, want to bring hamstring up
Kernig: brig up hamstring, want to flex neck.
(Releases tension on hamstrings)
Gall bladder - push on RUQ
-traps gallbladder between hand n liver
-pt cannot take a deep breath.
Venous blood gasses
BE -2 to 2
HCO3 change = pH change
HCO3 10 mEq = pH 0.15 (same direction)
Bicarbonate replacement therapy
(Weight kg/4) x BE
1/2 given IVP
1/2 given in L fluid / hr
Minute ventilation calculation & normal value
Ve = Vt x f (frequency)
Normal value: 6.0 LPM
Alveolar minute ventilation calculation & normal value
Va = (Vt - Vd) x f
Vd=dead space (.33Vt or 1ml/lb IBW)
Normal: 4.2 l/min
Attempting to blow off co2, adjust vent rate or volume?
Increase rate, decrease volume = decrease Va
Decrease rate, increase volume = increase Va
Normal anion gap
8-16 (w/o K)
10-20 (w/ K+)
4 primary suspects of metabolic acidosis
#1: lactic Acidosis
3. Renal failure
M - methanol
U - uremia
D - DKA
P - paraldehyde
I - isoniazide
L - lactate
E - Ethylene Glycol
S - Salicylate
How quickly can magnesium be administered?
1g / 30 minutes (sometimes faster)
Alveolar O2 pressure calculation
PAO2 = FiO2 (PBAR -PH2O) - 1.2 (PaCO2)
PBAR: barometric pressure
PH2O: waster pressure, constant (lung humidity: 100% =47 torr)
Aa-Gradient calculation, normal, slight shunt, definite shunt values.
PAO2 (alveolar O2 pressure) - PaO2 (ABGs)
Slight shunt: >10
Definite shunt: >20
Steps to improve PaO2
1. Assure adequate Va (Vt / rate)
2. Maximize FiO2
4. Invert I:E
Which blood type patient is most likely to produce a hemolytic reaction?
Type O patient - can only receive type O blood
What percentage of Hemolytic reactions will result in DIC?
Hemolytic reaction treatment
-Support hemodynamics (fluids & pressors)
-maintain renal perfusion (fluid & diuretics)
-prevent DIC (maintaining pressure & oxygenation)
Circulatory overload post blood administration cause
Blood is colloidal - draws fluid into vascular space
Fresh frozen plasma primary indications
-Coumadin therapy reversal
-Antithrombin III deficiency (prolonged heparin therapy)
-dilutional coagulopathy (>1 blood volume or 10 units PRBC)
FFP commonly given with PRBCs at what rate
1:4 with PRBCs until 10 units PRBCs in then 1:1.
Driven by coags (Pt/PTT) >1.5 - 1.8 x normal