Clinical Correlation 5 Flashcards
heat related exposure
core temp. >40 degrees celsius (104 F)
CNS sx’s
heat stroke
happens when heat generation (high temp, high humidity, activity level) outweighs heat dissipation
heat stroke
prolonged heat exposure (classical or exertional)
headaches
confusion
convulsion/collapse
sx’s of organ failure
heat stroke
key physical exam elements:
temp >40 C
tachycardia, tachypnea, and hypotension
CNS sx’s
dry mucous membranes
heat stroke
therapy/treatment includes:
ABC’s
manage organ dysfunction
cooling
ice bath
avoid antipyretics and shivering (adverse effects)
heat stroke
acute/chronic ingestion
tinnitus, vertigo
hyperventilation
N/V/D
respiratory alkalosis
anion-gap metabolic acidosis
aspirin toxicity
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
anion-gap metabolic acidosis (for aspirin toxicity)
vomiting, tinnitus, vertigo, lethargy, seizure, hyperpnea (deep breathing), hyperthermia
sx’s of acute ingestion of aspirin
in elderly, has prescription meds w/ ASA, confusion, signs of dehydration
sx’s of chronic ingestion of aspirin
both acute and chronic ingestions of aspirin can lead to what on lung exam
crackles (edema)
check arterial blood gas and salicylate level; anion-gap w/ metabolic acidosis (Na+ - Cl + HCO3-)
to diagnose aspirin toxicity
therapy/treatment:
ABC’s
IV sodium bicarbonate
activated charcoal (absorbs pill fragments)
urinary alkalinization (excretes pill fragments)
hemodialysis
aspirin toxicity
deliberate or accidental ingestion
elevated APAP level
early: mild GI upset followed by liver damage (1-2 days)
late: severe hepatic dysfunction and necrosis
acetaminophen toxicity (APAP)
most common cause of acute liver failure
acetaminophen toxicity (APAP)
usually metabolized safely by glucuronidation and sulfation
APAP
assists in conversion to non toxic metabolite (dealing with APAP)
Glutathione
when this is depleted, acetaminophen is converted to toxic metabolite
glutathione
deals with different phases, with phase IV being the worst and liver damage/death
acetaminophen toxicity
phase sx’s:
asymptomatic
N/V
phase I
phase sx’s:
abd pain
jaundice
phase II
phase sx’s:
worsening abd pain and jaundice
bleeding/bruising
encephalopathy (stroke)
phase III
phase sx’s:
worsening or improving sx’s
if worsened, can lead to death
phase IV
physical exam findings:
jaundice
hepatomegaly
RUQ tenderness
bleeding/ecchymosis
lethargy
hypotension
hyperpnea
acetaminophen toxicity
to diagnose:
check serum APAP level
liver assessment CMP(bilirubin, albumin, PT/INR, and AST/ALT)
acetaminophen toxicity
therapy/treatment:
activated charcoal
N-acetylcysteine
acetaminophen toxicity
intermittent flushing
pruritis (itchy)
abd pain
gastritis
diarrhea
tachycardia and hypotension
mastocytosis
exists in 2 forms:
cutaneous (more common in children)
systemic (more common in adults)
mastocytosis
caused by Asp to Val substitution of KIT (which encodes a stem cell factor receptor)
mastocytosis
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
mastocytosis
key history elements:
GI: gastritis, cramps and diarrhea
Skin: flushing, itching, rash
mastocytosis
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
mastocytosis
to diagnose:
clinical signs
tryptase level
KIT mutation test
cutaneous biopsy
bone marrow biopsy (systemic)
mastocytosis
therapy/treatment:
H1 and H2 antihistamines
mast cell stabilizers
leukotriene/prostaglandin inhibitors
epi pen
mastocytosis
autosomal dominant inheritance that deals with no-itch swelling
hereditary angioedema
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
hereditary angioedema
no mast cell activation
deficiency of C1 inhibitor that causes inappropriate release of bradykinin (mediator of edema)
hereditary angioedema
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)
hereditary angioedema
key physical exam:
angioedema
asymmetric swelling
stridor, drooling
abd pain
hereditary angioedema
to diagnose:
check C4 level
C1 inhibitor function
genetic testing (AD)
hereditary angioedema
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)
hereditary angioedema
