exam 2 Flashcards
koebner phenomenon
- trauma to an area on skin -> psoriatic patch
auspitz sign
- if you peel of silvery scaling in psoriasis it will bleed
nikolsky sign
- press edge of bullae/ vesicle and top epidermal layer separates
treatment for drug eruptions
- d/c offeding agent
- antihistamines around the clock
- topical steroids BID for pruritis
- PO prednisone if bad
SJS and TEN
- TEN covers 30% or more of total body surface area
- skin comes off in sheets
- mucosal loss
- admit to burn unit/ ICU
common causes of SJS or TEN
- phenytoin
- carbamazepine
- piroxicom
- allopurinol
- vaccines
class I steroids
- very potent
- severe non-facial and non- intertriginous areas
- scalp, palms, soles, on thick plaques
- use for < 4 weeks
- i.e. clobestasol
class II steroid
- high potency
- used on non-facial and non-intertriginous areas
- i.e. mometasone, fluocinonide
class III-V steroids
- medium potency
- non-facial and non-intertrignous areas
- ok on flexor surfaces for short periods
- can use for < 6-8 weeks
- i.e. mometasone, triamcinolone
class VI-VII
- least potent
- used for larger areas, thinner skin
- face, eyelids, genitals
- limit to 1-2 weeks on face and eyelids to avoid atrophy
- i.e. desonide, hydrocortisone
steroid absorption
- better absorbed in areas of inflammation and desquamation
- ointments have higher absorption and potency
- avoid occlusive dressings d/t atrophy and hypopigmentation
how do you dose steroids
- based on rule of 9s
- size of palm = 1% BSA
- dose 0.5 grams for 2% of BSA
- one finger tip= 0.5 grams
- one 30 gram tube will cover an entire adult body
how should you treat hair and nail fungal infections
- systemic anti-fungals
- dont respond well to topicals
what is the best treatment for candida
- nystatin
- not absorbed well in GIT
- candida= yeast normally found on mucous membranes, GIT and skin
what is the best treatment for dermatophytes
- allylamines
- naftifine
- terbinafine
- butenafine
stage I HTN
- 130-139/ 80-89
stage II HTN
- > 140/90
lifestyle modifications to treat HTN
- Na restriction to < 1500 mg/day
- weight loss
- exercise- 90-150 min a week
- mod alcohol intake
- eating K-rich foods
how much impact do lifestyle modifications have on BP?
- each likely to reduce SBP by 3-8 mmHg, DBP by 1-4 mmHg
what meds should pts with HTN avoid
- NSAIDs
- decongestants
- amphetamines
thiazide diuretics
- net loss of Na and water in urine
- after 4-6 weeks of tx Na balance and CO regained but BP remains low
- decreases TPR because Na causes vascular stiffness
- average fall in BP on low dose is 10 mmHg
how long does HCTZ work
- 24 hours
were do thiazide diuretics work
- distal convoluted tubules
ADRs of thiazide diuretics
- hypokalemia -> possible torsades and sudden death
- hyperglycemia
- hyperlipidema (stroke risk)
- hyperuricemia
at what doses are metabolic effects seen for thiazides
- high doses- 50-100 mg/ day
- dont see them at low doses of 12.5-25 mg
name the thiazide diuretics
- HCTZ
- chlorthalidone
- metolazone
- indapamide
- chlorothiazide
name the loop diuretics
- furosemide/lasix
- torsemide
- bumetanide
- ethacrynic acid
where do loop diuretics work
- loop of henle/ thick ascending limb
what are the classes of k sparing diuretics
- aldosterone antagonists
- Na channel blockers
list the aldosterone antagonists
- spironoloactone
- eplerenone
list the Na channel blockers
- amiloride
- triamterene
where do k sparing diuretics work
- collecting ducts
when is renin secreted and from where?
- secreted from kidneys
- decreased arterial BP
- decreased Na
- increased sympathetic activity
what does renin act on?
- angitensinogen to convert it to angiotensin I
how do you get angiotensin II?
- angtiotensin I converted to angiotensin II via ACE
main role of angiotensin II
- powerful vasoconstrictor
- causes aldosterone release -> Na retention
- mainly concerned about the ATI receptor
other effects of angiotensin II
- vasoconstriction of renal arterioles -> glomerular damage
- decreased NO release
- decreased fibrinolysis in blood
- increased thirst
- mitogenic effect- cell proliferation
overall “bad” effect of angiotensin II
- volume overload and increased TPR
- cardiac hypertrophy/ remodeling
HTN - myocardial infarction
- renal damage
- CV morbidity and mortality