Medicine Part 2 Flashcards
Most common causes of ESRD
Diabetes
HTN
How is ESRD defined?
Not by BUN or Cr
Loss of kidney function leading to clinical and lab findings of uremia
Calciphylaxis
Hyperphosphatemia –> calcium adn PO4 precipitate –> vascular calcifications –> skin lesions/necrosis!
Absolute indications for dialysis
AEIOU
Acidosis
Electrolytes - HYPERkalemia
Intoxications - methanol, eth glycol, lithium, aspirin
Overload - hypervolemia that can’t be solved
Uremia - based on clinical presentation, like pericarditis
Microscopic hematuria usually
glomerular in origin
Gross painless hematuria usually
Bladder or kidney cancer
Hematuria
> 3 erythrocytes / HPF on UA
Order to evaluate proteinuria
Urine dipstick - specific for albumin
UA
Dipstick + blood
UA no RBC
What is it?
Hemoglobinuria
Myoglobinuria
Proteinuria
> 150 mg protein/days
Glomerular d/o vs tubular d/o
In glomerular but not in tubular:
- need biopsy usually
- steroids and immunosuppressive meds for tx
In tubular but not in glomerular:
- acute presentation,
- caused by toxins
- does not cause nephrotic syndrome
Acute Interstitial Nephritis
- features
- seen on labs
- causes
Polyruia and sterile pyruria (maybe some WBC casts) are early manifestations
acute interstitial renal inflammation + pyuria + eosinophils (hypersensitivity) + azotemia
happens after drugs METHICILLIN #1 NSADs captopril penicillins sulfonamides rifampin TMP cephalosporins
AIN treatment
Remove offending agent
Steroids if still getting worse
Acute tubular necrosis
- causes
- stages
Toxic (#1 aminoglycosides) or Ischemic (more serious, prerenal azotemia usually (shock, sepsis) or crush injury w/ myoglobinuria) → granular casts (muddy brown)
o This is medullary necrosis and ATN is limited to outer medullar segments b/c renal medulla is susceptible to ischemic injury b/c low medullary blood flow → glomeruli look normal
o Stages: (1) inciting event → (2) Maintenance (oliguric, risk of hyperkalemia & met acidosis) → (3) Recovery (polyuric, risk of hypoK)
Nephrotic syndrome
- features
o Hyperlipidemia b/c increased hepatic lipoprotein synth – but only LDL; HDL will decrease!
o Hypoagammaglobinemia = increased risk infection
o Hypoalbuminemia = edema
o Hypercoagulable = loss antithrombin 3
Minimal change disease
-only lose albumin, not all globulins
Diffuse cortical necrosis
usually due to hypOperfusion of kidney (vasospasm, DIC, abruption placentae, septic shock), medulla spared
Renal papillary necrosis
- what is it
- causes
- dx
necrosis of renal papillae (supplied by vasa recta) = hematuria, proteinuria
o “POSTCARDS” = Pyelonephritis, Obstruction, Sickle Cell, TB, Cirrhosis, Analgesic abuse (phenacetin, acetaminophen, aspirin), Renal transplant rejection, Diabetes (#1), Systemic vasculitis
o DACS = Diabetes Mellitus (#1), Acute pyelonephritis, Chronic phenacetin use (acetaminophen), Sickle Cell
Dx w/ ecretory urogram - note change in papilla or medulla
Acute renal failure
↓ renal function → ↓GFR → INCREASE BUN and Creatinine (azotemia)
will also have met acidosis!
Chronic renal failure
Hyper K (#1 COD b/c arrhythmia) Metabolic ACIDosis (increase H+, ↓ bicarb) Uremia Anemia renal osteodystrophy dyslipidemia Na/H2O retention growth retardation in children;
FREE Ca will be decreased b/c increase in PO4 will bind up the free Ca in blood
Renal tubular acidosis
D/o of renal tubules –> nonanion gap HYPER Cl metabolic acidosis
Glomerular function OK
decrease in acid excreted in urine
Type 1 RTA
- what is it?
Distal
Can’t secrete H+ at distal tubule –> new bicarb cannot be made
Urine pH does not go below 6
Type 1 RTA
- effects of it
Decrease ECF
Hypo K, HYPER Cl, met acidosis
Renal stones
Type 1 RTA
- causes
MM
Nephorcalcinosis
Amphotericin B
Lupus, Sjorgen’s
Medullary sponge kidney
Analgesics
Type 2 RTA
- waht is it?
Proximal
Can’t reabsorb HCO3 at PCT –> more bicarb excreted in urine
Type 2 RTA
- effects
Hypo K, HYPER Cl, met acid
NO KIDNEY STONES
Type 2 RTA
- causes
Fanconi's syndrome Wilson's Lead toxicity Amyloid MM
Type 4 RTA
Hypoaldo or resistant to aldo
Decreased Na absorbtion + decreased H and K secretion in DCT
HYPERkalemia (not hypo) + acidic urine + met acidosis
Hartnup syndrome
AR
defective aa transporter
Tryptophan can’t be reabsorbed –> NAD deficiency
Dermatitis, diarrhea, ataxia, psych disturbances (all like pellagra)
Supplement w/ NAD if symptomatic
Fanconi’s syndrome
PCT dysfunction
can’t transport
- glucose
- aa
- Na
- K
- PO4
- uric acid
- bicabr
Results in
- rickets
- osteomalacia, osteoporosis
- polyuria,
- dehydration
- type 2 RTA
- hypercalciuria
- hypo K
Dx ADPKD
Ultrasound
Can use CT and MRI
Extrarenal involvement of ARPKD
Liver - protal HTN, cholangitis
Pulm insufficiency - pulm hypoplasia + enlarged kidneys - mostly because not enough amniotic fluid
Potter syndrome
Medullary sponge kidney
Cystic dilation of CD
can be assoc w/ hyper PTH and parathyroid adenoma
Benign; some stones and more UTI sometimes
Dx medullary sponge kidney
Intravenous pyelogram - inject contrast to see on xray
Renal artery stenosis
- causes
Atherosclerosis (31)
Fibromuscular dysplasia
- usually in young fems
- bilateral in 50% ppl
Dx renal artery stenosis
Renal arteriogram
- DO NOT USE FOR RENAL FAILURE. Contrast can be nephrtoxic
MRA - ok for renal failure
Renal vein thrombosis
- when is it seen?
RCC invasion
Nephrotic syndrome
Preggers/OCP
Dx renal vein thrombosis
renal venography
IVP
Where does sickling of sickle cell most commonly occur in kidney?
Renal papille
Can get papillary necrosis, renal fail, lots of UTIs
ACEI can help
Causes of hyperoxaluria
Steatorrhea
Small bowel disease
Crohns
Pyridoxine deficiency
Initial test to dx urinary tract obstruction
Renal ultrasound
Gold standard to dx urinary tract obstruction
Intravenous urogram (IVP)
NOT for preggers, allergies to contrast
PSA
DRE
Transrectal ultrasonography (TRUS)
- what do you do with these results when screening for prostate cancer?
PSA > 10 —> Do TRUS w/ biopsy
DRE abnormal —> Do TRUS w/ biopsy
PSA < 4 + DRE (-) —–> annual f/u
4.1 < PSA < 10 + DRE (-) —–> biopsy
DRE of prostate cancer
Prostate hard, nodular, irregular
PSA of cancer vs PSA normal
PSA cancer usually bound by plasma proteins
PSA normal usual free in plasma
Risks for RCC
Cigarettes Phenacetin analgesics ADPKD Chronic dialysis Mercury Cadmium HTN
Dx RCC
Renal US only detects mass
Abdominal CT (w/ and w/o contrast) - for dx and staging
Tx RCC
Radical nephrectomy
Take out:
kidney
adrenal
Gerota’s fascia
Transitional cell caricinoma
Can be anywhere along kidneys –> ureter
Mostly in bladder
Frequently recurs
TCC risk factors
Pee SAC
Phenacetin
Smoking (#1)
Aniline dyes
Cyclophosphamide
Dx TCC
Cystoscopy + biopsy (definitive)
Staging of TCC
CXR
CT scan
Testicular cancers
- Germ cell tumors
Most common
Seminomas
- radiosensitive, slow growing
Embryonal
- very malignant, mets early
Choriocarcionma
- most aggressive, mets always
Teratoma
- usually no mets
Yolk sac
- rare, usually in kids
Testicular vs. scrotal cancers
Testicular cancers usually always malignant
Scrotal cancers usually benign
Testicular cancers
- Non germ cell tumors
Usually benign, less common
Leydig cells
- benign, tx w/ surgery
- secrete estrogens and androgens –> precocious puberty
Sertoli cells
- usually benign
Testicular cancer risk factors
Cryptochidism (risk still there w/ correction)
Kleingelter’s
Testicular ca tumor markers
B HCG
- increased in choriocarcinoma
AFP
- increased in embryonal tumors
US to try and localize tumor
DDx of testicular mass
Cancer
Varicocele
Torsion
Spermatocele
Hydrocele
Epididymitis
Lymphoma
Tx testicular cancer
Inguinal (not scrotal) excision of testicle
CT scan to stage
BHCG and AFP measurements
Penile cancer assoc
HSV
HPV 18
Testicular torsion
Surgical emergency
After 6 hrs, may have infarction and no longer save testicle
Epididymitis
Infection of epididymis
Usually E coli
Gonorrhea, Chlamydia in sex active
Fever
Less acute onset vs. torsion
Total body water
60-40-20
60% body wt = water
40% = ICF
20% = ECF
- 15% = interstitial
5% = plasma
What is impt to track to assess volume status?
Urine output
Normal kids = > 1 mL/kg/hr
Normal adults = 0.5-1 mL/kg/hr
Anascara
extreme generalized edema
Fluid replacement therapy options
NS
- increase intravascular volume if dehydrated
- not great for CHF
D51/2NS = 5% dextrose, 1/2 NS
- standard maintenance fluid
- dextrose to inhibit muscle breakdown
D5W
- dilute powdered meds
- only some stays intravascular b/c diffuses into TBW compartment; not great to replenish intravascular
Lactated ringer’s solution
- good to replacing intravascular volume
- NOT a maintenance fluid
- common trauma resuscitation
- DO NOT USE if hyperkalemia is concern b/c has K
Calculation of maintenance fluids
100.50.20 rule
For 70 kg man:
10 kg x 100
10kg x 50
50 kg x 20
Total: 2500
2500/24 = 104 mL/hr
Changes in Na concentration = ?
Changes in Na content =
Concentration –> reflection of water homeostaiss
Content –> reflection of Na homeostasis
Hyper/hyponatremia
vs
Hypo/hypervolemia
Hyper/hyponatremia caused by too little/too much WATER
Hyper/hypovolemia caused by too much/too little Na
Hypo Na symptoms
Usually neuro sx
Headache, delirium, irritability
Muscle twitching, weakness
Hyperactive deep tendon reflexes
Seizures, coma
N/V, watery diarrhea
HTN b/c increased ICP
Oliguria
Tx hyponatremia
- hypotonic hyponatremia
Mild (120-130)
- withhold free water
Moderate (110-120)
- loop diuretics + saline
Severe (< 110)
- hypertonic saline increasing serum Na by 1-2 mEq/L/hr
Risks of correcting hypoNa too fast
Central pontine demyelination
Risks of correcting hyper Na too fast
cerebral edema
Hyper Na symptoms
Neuro sx usually
AMS
restlessness
Weakness
Focal neuro deficits
What should be given to differentiate nephrogenic from central DI if DI suspected?
DesmopressiN
Hypoalbuminemia, Ca is low. But ionized Ca is normal.
How do you est ionized Ca
Total Ca - (serum albumin * 0.8)
What alters Ca binding to albumin?
pH changes
Increase pH –> increase binding of Ca
- decrease ionized Ca
- total Ca ok
Causes of decreased Ca
Hypo PTH Acute pancreatitis Renal insufficiency Hyper PO4 Pseuhypoparathyroidism Hypo Mg Vit D deficiency Malabsorb Blood transfusion w/ citrated blood Osteoblastic mets Hypoalbuminemia DiGeorge
Features of decreased Ca
Rickets, osteomalacia Tetany - Chovstek's, Trousseau's sign Seizures Basal ganglia calcifications Arrhythmias
PROLONGED QT`
Causes of increased Ca
Hyper PTH
Renal failure (usually hypo Ca but can be hyper w/ high enough PTH)
Acromegaly
Addison’s
Metastatic ca
MM
PTH paraneoplastic
Vit D intox
Milk alkali syndrome
Thiazides,, lithium
Sarcoidosis
Familial hypocalciuric hypercalcemia
Features of increased Ca
Stones Bones Groans Psych overtones ---> All increased PTH signs
POlydipsia, polyuria
HTN
Wt loss
SHORT QT
1st step in management of hyper Ca
Increase urinary excretion via IV fluids
Diuretics (furosemide) to stop Ca reabsorb
What can you use to quickly tell why someone is hypokalemic?
Presence or absence of HTN
HTN - aldo increased - causes K wasting
No HTN - GI or renal loss of K
Hypo K EKG
Flattened T wave/ T wave inversion
U wave
Does dig cause hyper or hypo K?
What predisposes to dig toxicity
Causes HYPER K
Hypokalemia predisposes - allows Dig to bind more to Na/K pump
Features of hypo K
Arrhythmias Muscle weakness, paralysis, cramps Paralytic ileus Polyuria adn polydipsia N/V
How best to replete K?
KCl
10 mEq KCl increases K by 0.1 mEq/L
Add lidocaine so KCl doesn’t burn as much
How fast can you infuse K?
10 meq/hr in periph IV line
20 meq/hr in central line
When do you correct hypo Mg first?
In both hypo K and Ca
How does hyper K affect kidneys to worsen acidosis?
Inhibits renal ammonia synthesis and reabsorb
Net acid excretion is impaired!
Metabolic acidosis
Further makes K move out of cells
Hyper K EKG
Peaked T waves
Prolonged PR interval
Widen QRS
–> eventually get QRS merge w/ T wave producing sine pattern
–>
Vfib
Tx Hyper K
IV calcium
- decreases membrane excitability
- be careful giving this to pts on dig b/c can worsen toxicity
Shift K into cell
- glucose + insulin (fastest)
- sodium bicarb (for emergencies)
Remove K from body
- Kayexalate (exchange resin)
- hemodialysis
- diuretics
Where is most of Mg in body?
Bones
Where is most of K in body?
Intracellular
Where is most of Na in body?
Extracellular
Causes hypo Mg
Malabsorb
Fasting
Fistulas
TPN
Alcoholism
SIADH Diuretics Bartter;s syndrome Gentamicin, amphotericin B, cisplatin, PPIs Renal transplant
DKA, burns, lactation
Hypo Mg features
Muscle twitching Weakness Tremors Hyperreflexes Seizures AMS
Hypo K and Ca
Hypo Mg EKG
Prolonged QT
T wave flattening
Torsades
Causes of hyper Mg
Renal failure
Burns, trauma, ECF volume deficit
Mg-laxatives, antacids
Adrenal insufficiency
Adnreal insufficiency
Rhabdomyolysis
Hyper Mg features
Nausea Facial paresthesias Deep tendon reflex LOSS Respiratory depression Coma
Hyper Mg EKG
Like hyper K
Increased PR
Widened QRS
Elecated T
Tx hyper Mg
No Mg
IV calcium gluconate
Saline + furosemide
Dialysis
Intubation if respiratory depression
Where is most of PO4 in body?
Bones
Causes of decreased PO4
DKA
Alcohol abuse
Hypo PO4 clinical features
Encephalopathy
COnfusion
Seizures
Paresthesias
Weakness
Myalgias
Rickets
Hemolysis
RBC dysfunction
Cardiomyopathy b/c low ATP
Rhabdomyolysis
Hyper PO4 causes
Renal insufficiency Bisphosphoates Hypo PTH Vit D intoxication Tumor calcinosis Rhabdo cell lysis acidosis
Hyper PO4 features
Metastatic calcification + soft tissue calcifications
Neuro changes from decreased Ca
Tx hyper PO4
PO4 binding antacids (Al OH or carbonate)
Hemodialysis
Which bicarb value is more reliable?
- serum vs. ABG?
Serum (venous) CO2
Salicylate OD acid base status
Respiratory Alkalosis
Metabolic acidosis
Causes of renal loss of bicarb
Proximal tubular acidosis
- MM
- cystinosis
- Wilsons
Distal tubular acidosis
- can’t make HCO3
- SLE, sjogren’s, amphotericin B
Acetazolamide
Causes of GI loss of bicarb
Diarrhea
Pancreatic fistulas
Small bowel fistulas
Ureterosigmoidostomy
Danger to tx acidosis w/ bicarb
Bicarb takes 24 hrs to get to brain
Hyperventilation is continuing though
PaCO2 low while HCO3 increases - dangerous
What can be used to clinically detect endogenous depression?
Dexamethasone suppression test
50% of pts w/ depression, DST will be abnormal
Hallmark of prolonged seizures
Cortical laminar necrosis
Can lead to persistent neuro deficits and recurrent seizures
Status epilepticus
Any 1 seizure > 5 mins
Cluster of seizures w/ pt not recovering normal mental stauts in between
Initial TB infection - what does it look like on CXR?
Peripheral pulmonary focus
- Gohn focus remains as calcified granuloma
Mediastinal or hilar lymphadenopathy on CXR
Hyposthenuria
Found in pts w/ sicklle cell + trait
Thought to result from RBC sickling in vasa rectae of inner medulla which impairs countercurrent exchange and free water reabsorb
Proximal muscle weakness
Spares muscles of mastication and facial expression
Dysphagia possible
What is this?
Polymyositis/Dermatomyositis
Muscle biopsy to dx
Large blunt hyphae
Thick walled budding spores
What is this?
Malassezia furfur
Causes tinea versicolor
Hypopogmented macules that do not tan
Do not appear scaly
Scale on scraping
What is this? How to tx?
Tinea versicolor
Topical selenium sulfide ltion
Ketoconazole shampoo
What do you expect in any pt w/ hx of cancer or fever who p/w back pain and neuro sx, particularly loss of bowel or bladder function?
How do you confirm dx?
What should you do 1st?
Compression of thecal sac
MRI to confirm
Glucocoritoicds (dexamethasone) to start asap so decrease risk of permanent neuro damage
Low leukocyte alk phos + leukocytosis
CML
Most impt modifiable factors for decreasing HTN
Wt control > physical activity > Na restrict > moderation of EtOH consumption
Waldenstroms macroglobulinemia
Plasma cell neoplasm
IgM spike –> hyperviscosity
Hepatosplenomegaly, lymphadenopathy Anemia --> tiredness Increased bleeding Night sweats headaches Dizziness Visual problems (retinal v engorgement) Pain and numbess in extremities --> demyelinating sensorimotor neuropathy
MM vs. Waldernstroms
MM has
IgA or IgG
Doesn’t have hyperviscosity
Big danger of pancreatic necrosis
Locally released pancreatic enzymes can increase vascular permeability w/in and around pancreas
Large volume of plasma into retroperitoneum
Hypotension mainly due to increase in vascular permeatbility!!!
Valvular consequence of aortic dissection
Best way to dx AD
Aortic regurg
Transesophageal echo (more than MRI b/c MRI is long)
Contraindicaitons to liver transplant
Irreversible cardio-pulm dz causing prohibitive risk
incurable or recent malignancy outside of liver
Active EtOH or IVDU
During acute asthma, what is one indicator of severe attack
Normal PaCO2
Should be decreased b/c hyperventilate
Normal to increased = CO2 retention b/c severe obstruct and/or respiratory muscle fatigue
How do you improve ARDS oxygenation
Increase PEEP w/ low tidal volumes on ventilator setting
How does a person get infected w/ cystercosis
If eat larvae in undercooked pork, will get intestinal infection
If eat eggs from human feces, cystercercosis happens
- larvae will invade intestinal wall adn can go to muscle, brain, subQ tissue, eye
NOT GOTTEN BY EATING INFECTED PORK AS THE ONLY WAY - POOP OF HUMAN!
When is AS symptomatic?
Valve area < 1 cm2
Systemic effects of sarcoidosis
ACE increase
Increase vitamin D
Antiphospholipid syndrome features
Arterial and venous thromoboses
Thrombocytopenia
Prolonged PTT
Avoid preggers loss w/ LMWH
Signs of glucocorticoid deficiency
Weakness
Fatigue
Loss of appetite
Eosinophilia
Presentations of P vera
HTN Increased peptic ulceration Gouty arthritis Plethoric face Splenomegaly Hypercellular bone marrow
Earliest renal abnormality in pts w/ DM
Glomerular hyperfiltration
ACEi reduce intraglomerular HTN –> decrease glomerular damage
This can eventually cause thickening of glomerular BM –> nodular sclerosis
Pneumonia + GI sx + elevated LFTs
What is this? How do you tx?
Legionella pneumoniae
Quinolone or macrolide ot tx
What is infection w/ Moraxella catarrhalis commonly assoc w/
COPD
PFTs in IPF
Decreased TLC
normal FEV1/FVC
Diffusing capacity decreased
Increased Aa gradient
Diagnostic criteria for ARDS
Acute onset
PaO2/FiO2 < 200
Bilateral infiltrates on CXR
Swann Ganz P < 18 mm Hg
What should FiO2 be if person is adequately venetillated to prevent O2 toxicity to lungs?
below 60%
Increase PEEP as needed to maintain adequate O2 after FiO2 lowered
Bilateral trigeminal neuralgia
Transient muscle weakness
What is this most likely?
MS!
MS is one of few conditions presenting w/ bilatearl trigminal neuraligia
Systemic issue w/ L sided endocarditis
Can send septic emboli to regions rich in blood supply (brain, kidney, livre, spleen)
R sided endocarditis more likely to cause septic pulm emboli
Lab values for portal HTN causing splenomegaly
Anemia
Thrombocytopenia
Expansile adn eccentric lytic area (soap bubble) in epiphysis
Pain, swelling, decreased ROM
Most get pathologic fractures
Giant cell tumor
How do you diagnose a pheochromocytoma?
CT scan
MRI better for extra adrenal catecholamine secretion
Mibg scan if cr shows nothing
Any wide complex tachyarrhythmia is what until proven otherwise?
Ventricular tachycardia
In an MI, what is your long term prognosis most influenced by?
What do you do to achieve this?
How quickly?
Duration of time that lapses before coronary blood flow restored
Use Percutaneous transluminal coronary angioplasty and fibrinolysis
- PCTA better
- should be done w/in 90 mins
Fibrinolytics should be done w/in 30 mints
Erythematous rash and maculopapular
Starts on face –> trunk and extremities
Lymphadenopathy (occipital and posterior cervical)
Arthritis in adult women
Maybe some conjunctivitis
What is this?
Rubella
Measles does not have arthritis
What are cholesterol emboli usually preceded by?
Angiography
Plaque is disrupted by catheter or guidewire
Blue toe syndrome Livedo reticularis (reddish-cyanotic reticular discoloration of skin) Acute renal failure Ab pain Sometime pancreatitis Eosinophils in blood DECREASED COMPLEMENT LEVELS
Cholesterol emboli
Infarction of
- medial vermis of cerebellum
- lateral cerebellum
Medial
- severe vertigo
- nystagmus
Lateral
- dizziness
- ataxia
- weakness
- tendedncy to sway towards side of lesion
Dizziness
Hearing loss
Tinnitus
Meniere’s disease
Pathophys of benign positional vertigo
Ca crystals in inner ear shift position
Nystagmus
Nausea
Vomitting
4 cardinal symptoms of rest less syndrome
Uncomfortable sensation/urge to move legs
Discomfort worse at night/sleep
Discomfort worse at rest
Discomfort helped by mvmt of affected limbs
Pathophys of RLS
Abnormalities of dopaminergic transmission in CNS
What vaccines should pts w/ chronic liver disease get?
Tdap (every 10) Influenza Pneumococcal vaccine (every 5) Hep A Hep B
Major causes of vit K deficiency
Inadequate diet intake
Intestinal malabsorb
Loss of storage sites due to hepatocellular disease
How long does vit K storage last?
30 day
acutely sick - 7-10 days
Hemolytic uremic syndrome
Often follows diarrhea
Thrombocytopenia
MAHA
Fever
Renal failure (rather than neuro sx of TTP)
Shiga-toxin binds to the globotriaosylceramide (Gb3) receptor on the surface of the glomerular endothelium
This action includes a cascade of signaling events leading to apoptosis and binding of leukocytes to endothelial cells.
The Shiga-toxin-activated endothelial cells then become thrombogenic (clot-producing)
Additionally, the binding action of Shiga-toxin inactivates a metalloproteinase called ADAMTS13
What should all pts w/ significant bladder outlet obstruction get?
Foley catheter
Prolonged obstruction > 2 weeks can results in permanent kidney damage
How do you best view an acoustic neuroma?
MRI w/ contrast
DO NOT miss this as reason for hyperkalemia in an asymptomatic pt
Pseudohyperkalemia
- venipuncture can hemolyze RBC –> cause K to be released
When do you tx hyperkalemia?
How do you do it?
If cardiac toxicity (EKG shows), muscular paralysis, K > 6,5
+ Ca gluconate to stabilize myocardial membrane
- push K into cells w/ insulin and/or B-agonists
- can also use Na Bicarb to shift into cells
Nonhealing ulcer
Scaling plaque w/ central ulceration
Biopsy shows polygonal cells w/ atypical nuclei at all levels of epi w/ zones of keritnization
What is this?
Squamous cell carcinoma of skin
Sunlight is risk factor
Personality changes Compulsive behaviors Impaired memory Visuospatial functions intact \+ family hx in some
What is this?
Frontotemporal dementia (Pick’s disease)
Fluctuating cognitive impairment
Bizarre, visual hallucinations
Some parkinsonism but poor response to D agonist therapy
What is this?
Lewy body dementia
Eczematous lesion on breast
Biopsy = large cells that appear to be surrounded by clear halos
What is this?
Paget’s disease of breast
Usually represents underlying adenocarcinoma
Halo cells b/c cancer cells become retracted from adjacent keratinocytes
Corneal sensation is via which nerve?
CN 5 - Trigeminal
3 most common causes of chronic cough (> 8 weeks)
Post nasal drip
Asthma
GERD
Steps to tx ascites
Na and water restriction
Spironolactone
Loop diuretic (not more than 1 L/day of diuresis)
Frequent abdominal paracentesis (2-4L/day if renal function ok)
When are vascular shunts for liver cirrhosis indicated?
Symptomatic varices
Side to side porto caval shunt to help ascites but worsens encephalopathy
Peritoneo jugular shunt tx ascites
Indications for hemodialysis
Refractory hyper K
Volume overload/pulm edema NOT responding to diuretics
Refractory met acidosis (pH < 7.2)
Uremic pericarditis
Uremic encephalopathy or neuropathy
Coagulopathy due to renal failure
Best to tx frostbite
Rapid re-warming w/ warm water (40-44)
Result in less tissue damage than slow rewarming
Osgood Schlatter disease
Overuse injury caused by repetitive strain
Young kids w/ rapid growth spurt
Avulsion of apophysis of tibial tubercle
1 COD in dialysis pts
Cardiovascular disease
GERD hx
- progressive dysphagia to solids w/o anorexia or wt loss
Benign strictures
GERD hx
- progressive dysphagia to solids w/ anorexia or wt loss
- GERD for > 20 years
Adenocarcionma of esophagus
Charcot’s joint
Neurogenic arthropathy
Usually in diabetic neuropathy
Complication of neuropathy and repeated joint trauma
Affects wt bearing joints –> functional limitation, deformity, degenerative joint disease
Persistent ST segment elevation after recent MI and deep Q waves in same leads
Ventricular aneurysm
Causes of pulsus paradoxus
Cardiac tampanode
ASthma
COPD
–> in pulm conditions b/c extra negative pressure gets more blood into lungs, further decreasing LV preload
What prevents development of pulsus paradoxus even in presence of pericardial effusion and cardiac tamponade?
Signficiant arotic regurg – causes large increase in LVEDP preventing septum shift
Pts w/ hyper PTH increased risk of developing what arthropathy?
Pseudogout - CPPD deposition
Dx lactose intolerance
Lactose hydrogen breath test
Increase H level after eat lactose –> indicates bacterial carb metabolism (as lactose no absorbed by gut so bacteria get to it)
Waddling gait
Muscular dystrophy
- weakness of gluteal muscles
Spastic gait
Lesions of UMN
Slow, stiff, effortful movements
Wide based high stepping gait
Loss of proprioception
Dorsal roots or posterior column damage
Pathology of angioedema
C1 inhibitor deficiency, dysfunction or destruction
Leads to increased C2b and bradykinin = edema producing factors
C4 levels are depressed
erythema nodosum - what is it?
Infection of fat cells
It is a panniculitis
When are you at risk for hypocalcemia due to citrate chelation
If transfuse > 1 unit/5 min
Live failure b/c liver processes citrate
Definition of HTN
- in gen pop
- in diabetics and renal disease
Gen pop > 140/90
Diabetes and renal disease > 130/80
Emergency eval of headache
Noncontrast CT to rule of ICH
Small bleeds may not show up - LP can be done if high suspicion and no bleed shown
Which headache is most responsive to ppx?
Cluster headaches
– use verapamil
Pt w/ migraines but do not respond to drugs for tx migraines. What are they?
Rebound analgesic headaches
Try and wean from analgesics!
Do you need antibiotics for bronchitis?
NO! Usually viral
Causes of laryngitis
Usually viral
Moraxella catarrhalis, H influenzae
Sore throat Ddx
Viral infection
Tonsilitis
Strep throat
Mononucleosis
When should a pt w/ GERD be screened for Barrett’s
Symptomatic for at least 5 yrs
What Pulm finding are you at risk for w/ GERD?
REcurrent aspirationi pneumonia
you can find lipid laden macrophages in cytology
Need ppx for dental procedures for these groups
- Prosthetic cardiac valves
- History of prior infective endocarditis
- Unrepaired cyanotic congenital heart disease
- Completely repaired congenital heart disease for 6 months following repair
- Repaired congenital heart disease with residual defects or abnormalities
- Cardiac transplantation recipients with cardiac valvulopathy
How to tx small focal breast cancer
Lumpectomy w/ sentinel lymph node biopsy
Irradiation
1st degree family hx colorectal cancer - what’s the screening procedure?
Age 40
OR
10 yrs younger than 1st diagnosis
1st degree heart block
First-degree atrioventricular block is diagnosed when the PR interval is greater than 0.20 sec
EKG of WPW
PR interval (<0.11 sec), prolonged QRS duration, and slurred onset of the QRS (delta wave) complex.
Chronic alcoholism pts have risk of what electrolyte abnormality if they get admitted?
Hypo phosphate
Can be normal on admissions and decrease over first 12 to 24 hrs. Possibly because of IV glucose admin
Manifestation of rapid decrease in phosphate
Confusion
Rhabdomyolysis
Hemolytic anemia
Muscle weakness
Tx gallstone pancreatitis
ERCP with sphincterotomy and stone extraction
Orthostatic prteinuria
Increase in urinary protein excretion only in uprivht psiion
Most common in yong adults or children
Urine aniongap formula
Normal value
= (U sodium + U potassium) - U chloride
How do you tell if metabolic acidosis is of renal or extrarenal origin just by labs?
Extrarenal causes of metabolic acidosis are associated with an appropriate increase in net acid excretion primarily reflected by high levels of urine ammonium excretion, whereas kidney causes of this condition are associated with low net acid excretion and decreased urine ammonium levels.
Can get Urine ammoium w/ urine anion gap
Metabolic acidosis of extrarenal origin is suggested by a large, negative UAG caused by significantly increased urine ammonium excretion. Conversely, metabolic acidosis of kidney origin is suggested by a positive UAG related to minimal urine ammonium excretion.
If pt w/ polymyagia rheumatica has a prednisone taper 2x but keeps getting flares, what should be done?
Add steroid sparing agent and incease prednisone
Example ismethoteate.
When do you need a TTE for a murmur?
3/6 or greater systolic murmur
Diastolic murmur
Continuous murmur
New murmur if last PE was healthy
PR interval length
120 to 200ms
No more than 1 large box
QRS length
80 to 120ms
3 small boxes
QT interval
< 1/2 of R-R interval
How to tell the earliest if someone has rheumatoid arthritis?
A radiograph showing marginal joint erosions would most likely support a diagnosis of rheumatoid arthritis (RA).
Erosions of cartilage and bone are cardinal features of RA. Erosions and joint-space narrowing may develop as early as 2 to 3 mos
Where do you find rheumatoid factor?
RA
Hep C
Histo of Acute promyelocytic anemia
predominant cell is a large immature granulocyte with multiple granules overlying the cytoplasm and nucleus.
AML diagnosis
The diagnosis of AML is confirmed by a bone marrow aspirate showing hypercellular marrow containing greater than 20% to 30% myeloblasts.
Once the diagnosis of acute leukemia is established, the classification is based on the morphology of the immature cells.
The presence of Auer rods confirms the myeloid nature of the leukemia.
ALL features
lymphocytosis, neutropenia, anemia, thrombocytopenia, lymphadenopathy, and hepatosplenomegaly at presentation.
An increased number of lymphoblasts found on bone marrow examination are suspicious for the diagnosis.
When to screen for asymptomatic bacteruria
pregnant women
before urologic surgery
Pt w/ TB - suggestive pleural effusion. How do you best evaluate next?
Pleural biopsy
Is a duodenal ulcer cancerous?
No
Most common causes of gastric ulcers
NSAIDs
H pylori
Diabetic retinopathy classifications
nonproliferative (with hard exudates, microaneurysms, and minor hemorrhages), which is not associated with visual decline
proliferative (with “cotton-wool spots” and neovascularization), which is associated with loss of vision.
The presence of hypotension, hyponatremia, and a decreased urine sodium excretion accompanied by a bland urine sediment raises suspicion for…..
Prerenal azotemia
Tumor lysis syndrome may manifest as what electrolyte abnormalities?
hyperkalemia
hyperphosphatemia
hyperuricemia.
Meniscal tear vs. ligament injuries (ACL)
Swelling faster in ligament injuries
Click/knock of joint w/ loose cartilage
Pain on walking
What could have happened? what tests do you do to figure this out?
Meniscal tear
Pain along the joint line is 76% sensitive for a meniscal tear
an audible pop or snap on the McMurray test is 97% specific for a meniscal tear.
McMurray test
Maximally flexing the hip and knee and applying abduction (valgus) force to the knee while externally rotating the foot and passively extending the knee
Suspect common bile duct stone for sx of pancreatitis and jaundice. But none seen on US. What do you think it is?
Abdominal ultrasonography has a sensitivity of only 50% to 75% for choledocholithiasis, and a common duct stone should be suspected in the correct clinical situation even when ultrasonography does not show a stone
