Review Flashcards
(129 cards)
cutaneous drug reactions
- most cutaneous drug reactions are self-limited if DC’d
- triggers: foods, insect bites, drugs, enviro, exercise, infx
TYPE I: IgE MEDIATED (URTICARIA + ANGIOEDEMA)
TYPE II: CYTOTOXIC, AB-MEDIATED (drugs in combo w/ cytotoxic antibodies cause cell lysis)
TYPE III: IMMUNE ANTIBODY-ANTIGEN COMPLEX (drug-mediated vasculitis and serum sickness)
TYPE IV: DELAYED (CELL-MEDIATED) - morbilliform reaction (erythema multiforme)
- sx:
- EXANTHEMATOUS/MORBILIFORM RASH: MC SKIN ERUPTION - “bright-red” macules and papules that coalesce to form plaques; typically begins 2-14 days after med initiation (abx, nsaids, allopurinol, thiazides)
- URTICARIAL: 2nd mc type; occurs w/in minutes to hours after drug admin (abx, nsaids, opiates, radiocontrast)
- ERYTHEMA MULTIFORME: 3rd mc; target lesions may not always be present (sulfonamides, penicillins, phenobarbital, dilantin)
- FEVER, ABDOMINAL OR JOINT PAIN MAY ACCOMPANY THE CUTANEOUS RX
- less common: acneiform, eczematous, exfoliative, photosensitivity, vasculitis
- tx:
- discontinue offending med
- Exanthematous/Morbiliform –> oral antihistamines
- Drug-induced Urticaria/Angioedema –> SYSTEMIC CORTICO, ANTIHISTAMINES
- Erythema Minor –> symptomatic tx
- Anaphylaxis –> epi
erythema multiforme
- TYPE IV HSN - acute self-limited
- skin lesions usually evolve over 3-5 days and last 2 wks
- mc in young adults 20-40y
-Associations: HSV MC, mycoplasma (esp kids), S. pneumo, SULFA DRUGS, BETA-LACTAMS, PHYNYTOIN, PHENOBARBITAL, autoimmune, malignancy
- sx:
- TARGET LESIONS, DULL “DUSTY-VIOLET”, PURPURIC MACULES/VESICLES OR BULLAE in center w/ pale rim and red halo; OFTEN FEBRILE
- EM Minor: target lesions distributed acrally; no mucosal membrane lesions
- EM Major: target lesions w/ INVOLVE MUCOUS MEMBRANE (oral, genital or ocular), more central lesions, NO EPIDERMAL DETACHMENT
- tx:
- symptomatic: dc drug, antihistamines, analgesics, skin care
- oral: STEROID, lidocaine, diphenhydramine mouthwash
burns
rule of nines - not used for 1st degree
-palm = 1% of TBSA
Minor burns:
<10% TBSA in adults
<5% TBSA in young/old
<2% full-thickness burn
-must be isolated injury
-must not involve face, hands, perineum, feet
-must not cross major joints; must not be circumferential
Major burns: >25% TBSA in adults >20% TBSA in young/old >10% full-thickness burn -involve face, hands, perineum, feet -crossing major joints, circumferential burns
Rule of Nines head/neck = 9% total back and front upper limbs = 9% each trunk = 36% total back and front genitals = 1% lower limbs = 18% each
burns
First: superficial
- epidermis
- dry, red, tender to touch
- cap refill intact
- heals w/in 7 days, no scarring
Second: superficial partial-thickness
- epidermis and superficial dermis
- red/pink, moist, weeping, blistering
- most painful of all types
- cap refill intact
- heals 14-21 days, no scarring but pigment change
Second: deep partial-thickness
- epidermis into deep dermis
- red, yellow, pale white, dry, blistering
- not usually painful, decreased 2 point discrimination
- absent cap refill
- heals 3w - 2mo, scarring common (may need graft)
Third: full-thickness
- extends through entire skin
- waxy, white, leathery, dry
- painless
- absent cap refill
- heals in months, doesn’t spontaneously heal well
Fourth
- entire skin into fat, muscle, bone
- black, charred, eschar, dry
- painless
- absent cap refill
- doesn’t heal well, usually needs debridement of tissues and reconstruction
IV Fluid Resuscitation: PARKLAND FORMULA
-LACTATED RINGERS 4ml/kg/%TSA - IV first 24h
(1/2 in 1st 8 hours and other 1/2 over next 16 hrs)
macular degeneration
rf: >50yo, caucasian, F, smoker
- mc cause of permanent legal blindness in elderly >75yo
- macula responsible for central vision and detail/color
-MC dry (atrophic) type: gradual breakdown; DRUSEN = small, round, yellow-white spots on outer retina (accum of waste products)
-wet (neovascular or exudative): new, abnormal vessels grow under central retina and leak blood –> scars
(rare and faster progression)
-sx: bilateral blurred or loss of central vision (detail/color), scotomoas (blind spots), metamorphosia (straight lines appear bent), micropsia (objects look smaller)
retinal detachment
Rhegmatogenous MC type: retinal tear –> retinal inner sensory layer detaches from choroid plexus
- mc predisposing factors: myopia + cataracts
- sx: photopsia (flashing lights) –> floaters –> progressive unilateral vision loss (curtain coming down) in periphery initially –> central vision loss
- dx: fundoscopy = retinal tear, +shafer’s sign (clumping of brown pigment cells in anterior vitreous humor (“tobacco dust”)
- OPTHO EMER - keep supine, no drops –> laser, cryotherapy, ocular sx
ludwig’s angina
cellulitis of sublingual and submaxillary spaces in neck
- MC 2ry to dental infx (anaerobes)
- sx- swelling/erythema of upper neck and chin w/ PUS ON FLOOR OF MOUTH
- dx- CT SCAN
- tx- AMP/SULBACTAM (unasyn) or PCN + metro or clinda
cretinism
CONGENITAL HYPOTHYROIDISM due to maternal hypothyroidism or infant hypopituitarism
- sx- macroglossia, hoarse cry, coarse facial features, umbilical hernia, weight gain
- mental devo abnormalities if not corrected
-tx- LEVOTHYROXINE
thyroid storm (thyrotoxicosis crisis)
POTENTIALLY FATAL COMPLICATION OF UNTREATED THYROTOXICOSIS USUALLY AFTER A PRECIPITATING EVENT (surgery, trauma, infx, illness, pregnancy)
-RARE (1-2% w/ hyperthyroid, high mortality 75%)
- sx- HYPERMETABOLIC STATE: PALPITATIONS, TACHY, A-FIB, HIGH FEVER, N/V, PSYCHOSIS, TREMORS
- dx- INC FREE T3/T4, DEC TSH (may be undetectable)
Treatment is:
1) beta blocker (propranolol)
2) thionamide (propylthiouracil or methimazole)
3) iodine solution
4) glucocorticoids (supportive - inhibits peripheral conversion of t4 to t3 and impairs thyroid hormone production)
- AVOID ASPIRIN (causes increased T3/T4)
myxedema crisis
EXTREME FORM OF HYPOTHYROIDISM
-MC IN ELDERLY WOMEN W/ LONG STANDING HYPOTHYROIDISM IN WINTER
- patient will have acute precipitating factor (infx, CVA, CHF, sedative/narcotics) AND undiagnosed HYPO, noncompliance w/ HYPO meds
- patient will show severe signs of HYPO: BRADYCARDIA, obtunded, hypothermia, hypoventilation, HYPOGLYCEMIA, HYPONATREMIA, HYPOTN
-labs will look like HYPO –> inc TSH, dec T4/T3
- tx- IV LEVOTHYROXINE (give even w/ high suspicion)
- ICU ADMIT, treat underlying, PASSIVE WARMING
Riedel’s thyroiditis
FIBROUS thyroid
FIRM, HARD, “WOODY” NODULE, may devo HYPO
+/- surgery
osteogenesis imperfecta
genetic mutation for type 1 collagen (necessary for bone integrity) - assoc w/ severe osteoporosis, spontaneous frx in childhood, BLUE-TINTED SCLERAE + PRE-SENILE DEAFNESS
Addison’s Dz / Primary
ADRENAL GLAND DESTRUCTION (LACK OF CORTISOL AND ALDOSTERONE)
- AUTOIMMUNE: MC CAUSE INDUSTRIALIZED COUNTRIES –> CAUSES ADRENAL ATROPHY
- INFECTION: MC CAUSE WORLDWIDE (TB, HIV) –> CAUSES ADRENAL CALCIFICATION
- vascular: thrombosis or hemorrhage in adrenal gland
- metastatic dz
- medications: KETOCONAZOLE, RIFAMPIN, PHENYTOIN
- sx-
- HYPERPIGMENTATION (inc ACTH stimulation of melanocyte-stim hormones))
- Dec Aldosterone: ORTHOSTATIC HYPOTENSION, HYPONATREMIA, HYPERKALEMIA, NON-GAP META ACIDOSIS, HYPOGLYCEMIA
- Dec Sex Hormones in Women: loss of libido, amenorrhea, loss of axillary + pubic hair
- dx-
- screen w/ am cortisol??
- SCREEN FOR ADRENAL INSUFFICIENCY: HIGH DOSE ACTH (COSYNTROPIN) STIM TEST (blood or urine cortisol measured before and after IM injection ACTH)
- normal –> rise in blood/urine cortisol levels after ACTH
- ADRENAL INSUFFICIENT –> LITTLE/NO INC IN CORTISOL
- CRH STIMULATION TEST: differentiates btw causes of adrenal insufficiency
- PRIMARY/ADDISON (ADRENAL) –> INC ACTH BUT LOW CORTISOL (opposite)
- secondary (pituitary) –> low ACTH and cortisol
-tx- HYDROCORTISONE 1ST LINE + FLUDROCORTISONE
(hormone replace = synth glucocorticoid and synth mineralocorticoid)
-replace TT for women (adrenals only place it comes from, men have testes)
Cushing’s
cushing’s SYNDROME = SIGNS/SX RELATED TO CORTISOL EXCESS
cushing’s DISEASE = CUSHING’S SYNDROME CAUSED SPECIFICALLY BY PITUITARY INC ACTH SECRETION
- exogenous: IATROGENIC –> LONG TERM TX (MC CAUSE)
- endogenous: CUSHING’S DZ (BENIGN PITUITARY ADENOMA OR HYPERPLASIA –> SECRETES ACTH)
- ECTOPIC ACTH (secretes ACTH - small cell lung cancer)
- ADRENAL TUMOR - cortisol-secreting adrenal adenoma
- sx- 2ry to excess cortisol + glucocorticoids
- CENTRAL (TRUNK) OBESITY, MOON FACIES, BUFFALO HUMP, SUPRACLAVICULAR FAT PADS
- WASTING OF EXTREMITIES, PROXIMAL MUSCLE WEAKNESS, SKIN ATROPHY, STRIAE, inc infx, hyperpigmentation
- HTN, WEIGHT GAIN, HYPOKALEMIA, ACANTHOSIS NIG
- depression, mania, psychosis
- ANDROGEN EXCESS: hirsutism, oily skin, acne, inc libido, amenorrhea
- dx-
- SCREEN:
- LOW-DOSE DEXAMTEHASONE SUPPRESSION: nrml response is cortical supression; NO SUPPRESS = CUSHING’S SYNDROME
- 24 HOUR URINE FREE CORTISOL
- SALIVARY CORTISOL (usually at night)
- DIFFERENTIATING:
- HIGH-DOSE DEXAMETHASONE SUPPRESS –>
- SUPPRESSION = CUSHING’S DZ
- NO SUPPRESSION = ADRENAL OR ECTOPIC ACTH-producing TUMOR
ACTH LEVELS:
- DECREASED ACTH –> ADRENAL TUMORS (produce high levels of cortisol, suppressing ACTH levels via HPA axis)
- NORMAL/INCREASED ACTH –> CUSHINGS DZ OR ECTOPIC ACTH-PRODUCING TUMOR (secrete ACTH independent of HPA axis)
-tx-
-Cushing’s Dz (pituitary) –> TRANSPHENOIDAL SX (alt radiation)
-Ectopic ACTH-secreting or adrenal tumors –> SURGERY
(KETOCONAZOLE in inoperable pt, dec cortisol product)
-Iatrogenic steroid therapy –> GRADUAL STEROID TAPER
hyperaldosteronism
Primary: RENIN-INDEPENDENT
- idiopathic or bilateral adrenal hyperplasia, MC, women
- CONN’S SYNDROME: ADRENAL ALDOSTERONOMA
Secondary: DUE TO INCREASED RENIN
- INC RENIN –> 2ry INC IN ALDOSTERONE VIA RAAS
- MC DUE TO RENAL ARTERY STENOSIS or dec renal perfusion (CHF, hypovolemia, nephrotic syndrome)
- sx-
- HYPOKALEMIA: muscle weakness, polyuria, fatigue, dec DTR, hypoMg
- HYPERTENSION: HA, flushing, NOT EDAMATOUS
- dx-
- labs: HYPOKALEMIA W/ METABOLIC ACIDOSIS (due to dumping K and H in exchange for Na)
- Screen: ALDOSTERONE:RENIN RATIO
- Definitive: Saline Infusion Test
- CT/MRI - look for adrenal or extra-adrenal mass
- tx-
- Conn’s Syndrome: EXCISION + SPIRONOLACTONE (blocks aldosterone)
- Hyperplasia: SPIRONOLACTONE, ACEI, correct electros
- Secondary (renovascular htn): ANGIOPLASTY DEFINITIVE, ACEI
pheochromocytoma
CATECHOLAMINE-SECRETING ADRENAL TUMOR –> SECRETES NOREPI AND EPI AUTONOMOUSLY AND INTERMITTENTLY
- triggers: sx, exercise, pregnancy, meds
- 90% benign
- sx- HYPERTENSION!!!
- “PHE” - PALPITATIONS, HEADACHES, EXCESSIVE SWEAT
- dx- INC 24h URINARY CATECHOLAMINES
- MRI/CT to visualize adrenal tumor
- labs: hyperglycemia, hypoK
- tx- COMPLETE ADRENALECTOMY
- PREOP a-BLOCKADE: PHEnoxybenzamine or PHEntolamine x7-14d –> followed by BB to control HTN
- DON’T INITIATE THERAPY W/ BETA-BLOCKADE to prevent unopposed a-constriction during catecholamine released triggered by surgery or spontaneously (life threatening HTN)
*cocaine mimics same effect, same tx
hyperprolactinemia
PROLACTINOMAS MC CAUSE, hypothyroid, acromegaly, cirrhosis, renal failure
- DOPAMINE ANTAGONISTS (bc dopa inhibits prolactin) - metoclopramide, promethazine, prochlorperazine, SSRIs, TCAs, cimetidine, estrogen)
- pregnancy, stress, exercise
- increased prolactin inhibits gonadotropinRH –> dec FSH/LH
- women: oligomenorrhea, amenorrhea, galactorrhea, infertile
- men: impotence, dec libido, hypogonadism, infertility
-dx- TSH, BUN/Cr, LFTs, B-hCG, prolactin, +/-MRI
- tx- stop offending drugs
- CABERGOLINE or BROMOCRIPTINE 1ST LINE (dopa agonists inhibit prolactin)
- surgical tx in select pt
DKA
INSULIN DEFICIENCY + counterregulatory hormonal excess in DM as RESPONSE TO STRESSFUL TRIGGERS:
-INFECTION MC, INFARCTION, NONCOMPLIANCE W/ INSULIN, dose change, undiagnosed
- cortisol stress hormone –> inc glucose + patients can’t meet demand of inc insulin requirements
- YOUNGER PT W/ TYPE 1 DM
insulin deficiency –> hyperglycemia, dehydration, ketonemia (high anion gap meta acidosis), potassium deficit
-sx- HYPERGLYCEMIA, ABD PAIN, KETOTIC BREATH, KUSSMAUL’S RESPIRATIONS, weak, fatigue, confusion, tachy, hypoTN, decreased turgor
-dx- PLASMA GLUCOSE: >250 Arterial pH: <7.3 mild --> <7.0 severe Serum Bicarb: 15-18 mild --> <10 severe Ketones: POSITIVE Serum Osmolarity: varies
-tx-
initial: ABC, mental status, vitals, vol status, screen for precipitating event
-IV FLUIDS CRITICAL 1ST STEP –> ISOTONIC 0.9% NS UNTIL HYPOTN RESOLVES –> 0.45% NS –> D5 0.45 NS to prevent hypoglycemia from insulin tx
-when the blood glucose is < 200 mg/dL, treatment involves adding dextrose to the intravenous fluids
-INSULIN (REG) - lower serum gluc –> dec gluconeogenesis, recuced ketone production
-POTASSIUM: despite serum K levels, pt is always total body K deficient (correction of DKA will cause hypokalemia) If serum K high, wait til normal and then replete
+bicarb if severe acidosis
metabolic syndrome
- dx - at least 3 of the following:
- dec HDL: <40 men, <50 women
- inc BP: >135 systolic or >85 diastolic (or meds for BP)
- inc fasting trigs: >150 (or meds for trigs)
- inc fasting blood sugar: >100 (or drug tx)
- inc abdominal obesity: waist circ >40” men, >35” women
MEN-1
Rare inherited disorder of 1+ overactive endocrine gland tumors (3 P’s) - most tumors are benign (esp <30yo)
PARATHYROID (90%), PANCREAS (60%), PITUITARY (55%)
-MEN 2a (90%): MEDULLARY THYROID CARCINOMA, PHEOCHROMOCYTOMA, HYPERPARATHYROIDISM
- MEN 2b (5%): medullary thyroid carcinoma, pheochromocytoma, NEUROMAS, MARFANOID
- assoc w/ presence of mucosal neuromas, and have a more aggressive form of thyroid cancer (presents in infancy)
schizophreniform disorder
meets criteria for schizophrenia but <6 mo duration
personality disorders
A - “ALONE” - not w/ social norms
B - “BATSHIT” - erratic, wild
C - “CONCERNED” - anxious
schizoid personality - HERMIT, ANHEDONIA, FLAT
schizotypal - APPEARANCE, INAPPROPRIATE AFFECT OR SPEECH, “MAGICAL THINKING”
antisocial - DEVIATING FROM NORMS, MAY COMMIT CRIMINAL ACTS, MAY BEGIN IN CHILDHOOD AS CONDUCT DISORDERS
paranoid
borderline - UNSTABLE, UNPREDICTABLE MOOD AND AFFECT, UNSTABLE SELF IMAGE AND RELATIONSHIPS, HARM TO SELF
histrionic - SELF-ABSORBED, TEMPER TANTRUMS, CENTER OF ATTENTION, SEXUALLY PROVOCATIVE, SEDUCTIVE
narcissistic - INFLATED SELF-IMAGE - CONSIDERS SELF SPECIAL, ENTITLED, REQUIRES SPECIAL ATTENTION BUT FRAGILE SELF ESTEEM
avoidant - DESIRES RELATIONSHIPS BUT AVOIDS RELATIONSHIPS DUE TO “INFERIORITY COMPLEX”
dependent - CONSTANTLY NEES REASSURANCE, RELIES ON OTHERS FOR DECISION MAKING AND EMO SUPPORT
ocd personality
treat benzodiazepine intoxication?
cocaine intoxication?
alcohol withdrawal?
FLUMAZENIL
BENZODIAZEPINE, neuroleptics and blood pressure reduction
- IV BENZOS –> POTENTIATES GABA-MEDIATED CNS INHIBITION (etoh mimics gaba at receptors)
- IV FLUIDS + THIAMINE + MAGNESIUM (PRIOR TO GLUCOSE ADMIN), multivitamins (B12/folate) - intoxication may cause hypoglycemia
renal cell carcinoma
tumor of proximal convoluted tubule (v metabolically active so most prone to dysplasia)