Clinical Correlation 5

Question 1

heat related exposure
core temp. >40 degrees celsius (104 F)
CNS sx’s

Answer 1

heat stroke

Question 2

happens when heat generation (high temp, high humidity, activity level) outweighs heat dissipation

Answer 2

heat stroke

Question 3

prolonged heat exposure (classical or exertional)
headaches
confusion
convulsion/collapse
sx’s of organ failure

Answer 3

heat stroke

Question 4

key physical exam elements:
temp >40 C
tachycardia, tachypnea, and hypotension
CNS sx’s
dry mucous membranes

Answer 4

heat stroke

Question 5

therapy/treatment includes:
ABC’s
manage organ dysfunction
cooling
ice bath
avoid antipyretics and shivering (adverse effects)

Answer 5

heat stroke

Question 6

acute/chronic ingestion
tinnitus, vertigo
hyperventilation
N/V/D
respiratory alkalosis
anion-gap metabolic acidosis

Answer 6

aspirin toxicity

Question 7

1.salicylates directly stimulate medulla
2. uncouples oxidative phosphorylation (so all other processes are activated to produce ATP)
3. increase in catabolism
4. accumulation of lactic acid
5. worsening neurotoxicity as pH decreases and crosses into brain

Answer 7

anion-gap metabolic acidosis (for aspirin toxicity)

Question 8

vomiting, tinnitus, vertigo, lethargy, seizure, hyperpnea (deep breathing), hyperthermia

Answer 8

sx’s of acute ingestion of aspirin

Question 9

in elderly, has prescription meds w/ ASA, confusion, signs of dehydration

Answer 9

sx’s of chronic ingestion of aspirin

Question 10

both acute and chronic ingestions of aspirin can lead to what on lung exam

Answer 10

crackles (edema)

Question 11

check arterial blood gas and salicylate level; anion-gap w/ metabolic acidosis (Na+ - Cl + HCO3-)

Answer 11

to diagnose aspirin toxicity

Question 12

therapy/treatment:
ABC’s
IV sodium bicarbonate
activated charcoal (absorbs pill fragments)
urinary alkalinization (excretes pill fragments)
hemodialysis

Answer 12

aspirin toxicity

Question 13

deliberate or accidental ingestion
elevated APAP level
early: mild GI upset followed by liver damage (1-2 days)
late: severe hepatic dysfunction and necrosis

Answer 13

acetaminophen toxicity (APAP)

Question 14

most common cause of acute liver failure

Answer 14

acetaminophen toxicity (APAP)

Question 15

usually metabolized safely by glucuronidation and sulfation

Answer 15

APAP

Question 16

assists in conversion to non toxic metabolite (dealing with APAP)

Answer 16

Glutathione

Question 17

when this is depleted, acetaminophen is converted to toxic metabolite

Answer 17

glutathione

Question 18

deals with different phases, with phase IV being the worst and liver damage/death

Answer 18

acetaminophen toxicity

Question 19

phase sx’s:
asymptomatic
N/V

Answer 19

phase I

Question 20

phase sx’s:
abd pain
jaundice

Answer 20

phase II

Question 21

phase sx’s:
worsening abd pain and jaundice
bleeding/bruising
encephalopathy (stroke)

Answer 21

phase III

Question 22

phase sx’s:
worsening or improving sx’s
if worsened, can lead to death

Answer 22

phase IV

Question 23

physical exam findings:
jaundice
hepatomegaly
RUQ tenderness
bleeding/ecchymosis
lethargy
hypotension
hyperpnea

Answer 23

acetaminophen toxicity

Question 24

to diagnose:
check serum APAP level
liver assessment CMP(bilirubin, albumin, PT/INR, and AST/ALT)

Answer 24

acetaminophen toxicity

Question 25

therapy/treatment:
activated charcoal
N-acetylcysteine

Answer 25

acetaminophen toxicity

Question 26

intermittent flushing
pruritis (itchy)
abd pain
gastritis
diarrhea
tachycardia and hypotension

Answer 26

mastocytosis

Question 27

exists in 2 forms:
cutaneous (more common in children)
systemic (more common in adults)

Answer 27

mastocytosis

Question 28

caused by Asp to Val substitution of KIT (which encodes a stem cell factor receptor)

Answer 28

mastocytosis

Question 29

Asp to Val substitution of KIT leads to gain of function mutation that is ligand independent (receptor is always turned on regardless)– clonal mast cell proliferation

Answer 29

mastocytosis

Question 30

key history elements:
GI: gastritis, cramps and diarrhea
Skin: flushing, itching, rash

Answer 30

mastocytosis

Question 31

key physical exam elements:
hypotension, tachycardia
wheezing (high pitched)
GI: abd tenderness, hepatomegaly, portal hypertension
Skin: red-brown macular or papular rash (urticaria pigementosa), Darier’s sign

Answer 31

mastocytosis

Question 32

to diagnose:
clinical signs
tryptase level
KIT mutation test
cutaneous biopsy
bone marrow biopsy (systemic)

Answer 32

mastocytosis

Question 33

therapy/treatment:
H1 and H2 antihistamines
mast cell stabilizers
leukotriene/prostaglandin inhibitors
epi pen

Answer 33

mastocytosis

Question 34

autosomal dominant inheritance that deals with no-itch swelling

Answer 34

hereditary angioedema

Question 35

episodic subcutaneous and submucosal non-pruritic (no itching) edema (tongue and lips swell)
episodic abd pain (GI swelling)
no hives or urticaria (rash)
sometimes mistaken for anaphylaxis

Answer 35

hereditary angioedema

Question 36

no mast cell activation
deficiency of C1 inhibitor that causes inappropriate release of bradykinin (mediator of edema)

Answer 36

hereditary angioedema

Question 37

key history elements:
swelling w/ NO itching
hoarseness
abd pain
sx’s of rash, tingling prior to edema
accused of drug-seeking (hard to see GI swelling)

Answer 37

hereditary angioedema

Question 38

key physical exam:
angioedema
asymmetric swelling
stridor, drooling
abd pain

Answer 38

hereditary angioedema

Question 39

to diagnose:
check C4 level
C1 inhibitor function
genetic testing (AD)

Answer 39

hereditary angioedema

Question 40

therapy/treatment:
ABC’s and supportive care
C1 inhibitor
blockage of bradykinin receptor (stop edema)
epinephrine and steroids have NO effect (b/c not histamine mediated)

Answer 40

hereditary angioedema