Family Medicine Shelf Flashcards
Four combinations of the tetanus vaccine
Children under 7yo: DTaP and DT
Children over 7 and adults: Tdap and Td
When do we give tetanus immunoglobulin
Only if the wound is severe or dirty AND the patient has not been vaccinated in the last 5 years against tetanus
- if the wound is clean and/or minor, no IG
When do we screen all pregnant women for asymptomatic bacteruria?
12-16 weeks
*bc it can progress to acute cystitis, acute pyelonephritis –> preterm birth, LBW
Treatment for asymptomatic bacteruria or acute cystitis in pregnant women
Nitrofurantoin 5-7 days
Amoxicillin or Augmentin 3-7 days
Fosfomycin single dose
*absolutely no Fluoroquinolones (cartilage) or TMP/SMX (congenital abnormalities, kernicterus)
Treatment for acute pyelonephritis in pregnant women
Hospitalize!
Give IV antibiotics (beta-lactams, meropenem)
Switch to 10-14 day course of oral antibiotics once she is afebrile for 24 hours
Treatment of acute cystitis or asymptomatic bacteria in pregnant women, if persistent after two more courses of antibiotics
Daily suppressive antibiotic therapy (nitrofurantoin) for the duration of pregnancy
Treatment for generalized social anxiety – pharm (2)
SSRIs (PAROXETINE) or SNRIs
+Cognitive behavioral therapy
Treatment for performance only social anxiety
Benzodiazepines or beta blocker 30 to 60 minutes before the performance
Cognitive behavioral therapy
*Avoid benzodiazepines if patient has history of substance abuse or does not want sedation
Sudden onset severe HA; worst HA Of my life
Subarachnoid hemorrhage
Three most common causes of clubbing
- Lung malignancy –> look for occult malignancy!!!
- Cystic fibrosis
- Right to left cardiac shunts
Pathophysiology of clubbing
Because of problems in pulmonary circulation –> Megakaryocytes failed to undergo normal fragmentation into smaller parts –> get stuck in the digital circulation –> begin to release PDGF and VEGF –> connective tissue hypertrophy + increased vascularity and permeability = clubbing
Zileuton (Zyflo)
5-lipoxygenase (Leukotriene) inhibitor
Montelukast (Singulair)
Leukotriene receptor antagonist
Jarisch-Herxheimer Reaction
Flu-like syndrome after starting antibiotics bc the killed bacteria start to release pyrogens (fever-inducing substances)
*classically seen in tx of spirochetes (syphillis, Lyme disease, leptospirosis, Q fever)
Blood on dipstick, but no RBCs seen on microscopy
Rhabdomyolysis
Normal body temp (Celsius vs Fahrenheit)
Celsius = 36-37.5 Fahrenheit = 96.8-99.5
Temp in heat stroke vs fever
Heat stroke temp > 104F (41C)
Fever temp >100.4
Uncontrolled effluent of calcium from sarcoplasmic reticulum = mechanism of what pathology?
Malignant hyperthermia
After admin of inhaled aesthetics like halothane and succinylcholine
Temps seen in malignant hyperthermia
> 113F (45C)
Main difference between anorexia nervosa and bulimia nervosa5
Anorexia = low body weight, BMI
Treatment for anorexia (3)
CBT
Nutritional rehabilitation
Olanzapine (if the first two don’t work)
Olanzapine - brand name and drug class
Olanzapine = Zyprexa Atypical antipsychotic (dopamine antagonist)
Treatment for bulimia nervosa
CBT
Nutritional rehab
SSRI (Fluoxetine = Prozac)
Russell’s sign (eating disorders)
Scars/calluses on hands/knuckles seen with repeated self-induced vomiting (hand scrapes against incisors)
Main difference btn bulimia nervosa and binge eating disorder
Bulimia has compensatory behavior (purging)
Binge eating disorder has NO compensatory behavior –> pt likely to be overweight
The three most common trisomies (# and name)
Trisomy 13 - Patau syndrome
Trisomy 18 - Edward Syndrome
Trisomy 21 - Down Syndrome
Trisomy 18 (Edwards Syndrome) signs (6)
Low birth weight Clenched fists (index overlaps 3rd digit, 5th digit overlaps 4th) Microcephaly Prominent occiput (back of head) Micrognathia (small jaw) Rocker bottom feet
Trisomy 13 (Patau syndrome) signs (5)
Cleft lip Flexed fingers + polydactyly Ocular hypotelorism (eyes close together) Bulbous nose Low-set malformed ears
Chromosomal deletion disease in which protruding metopic suture is characteristic
Cri-du-chat
5p deletion
Clomiphene citrate mechanism of action
Selective estrogen receptor modulator (SERM)
Antagonist at estrogen receptors in hypothalamus.
Prevents normal feedback inhibition of estrogen against LH/FSH –> causes increased release of LH and FSH from pituitary –> stimulates ovulation.
Used to treat infertility due to anovulation (e.g., PCOS).
May cause hot flashes, ovarian enlargement, multiple simultaneous pregnancies, and visual disturbances.
Ménière’s disease pathophys & signs
Abnormal fluid and ion homeostasis in inner ear –> distention of endolymphatic compartment in inner ear
Signs =
Episodic (20mins-24hours) Vertigo + sensorineural hearing loss and tinnitus
Horizontal nystagmus during acute attack
+/- postural instability & vomiting with the vertigo
Triggers of episodes in Meniere’s dz
Anything that causes endolymphatic retention!
Alcohol
Caffeine
Nicotine
**high salt foods (low salt intake is one of the lifestyle modifications)
Printzmental (variant) angina EKG changes
ST elevations during episode that return to baseline when episode ends
- contrast to MI where we have longer lasting ST elevations
- contrast to unstable angina where we have ST depressions
Young female patient with amenorrhea and other signs suspicious for Turner syndrome. First step in assessment
Pelvic ultrasound
Can show streak ovaries and infantile uterus
Mechanism of exercise induced amenorrhea
Low caloric intake:output –> low levels of GnRH and LH –> estrogen deficiency
**Hence why you get amenorrhea/infertility but ALSO, vaginal atrophy, breast atrophy, and osteopenia
Normal/acceptable PSA value
7ng/dL
Volume of urine seen on bladder scan that should make you think obstruction
> 100ml
Tamsulosin mechanism of action
Alpha-1 blocker –> causes smooth muscle relaxation –> hence use in BPH to allow urination
***selective for alpha receptors in prostate vs vascular alpha receptors
Finasteride mechanism of action
5-alpha reductive inhibitor –> blocks this enzyme that converts testosterone to DHT
*can be used in combination with alpha-1 blockers in BPH
Abnormal grid test: what is abnl, what pathology?
Grid test = grid of parallel vertical & horizontal lines
If patient sees the lines as wavy instead of straight = abnl result
Think MACULAR DEGENERATION (most common cause of visual loss in industrialized world)
NF2 signs (3)
Subcutaneous neurofibromas
Cafe-au-last spots
Hearing loss (usually bilateral, due to acoustic neuromas)
Inspiratory stridor that begins in neonatal period and is loudest by 4-8mos that is worse supine and better when prone
Laryngomalacia
Laxity of supraglottic structures causing stridor, reflux
Diagnosis and tx of laryngomalacia
Diagnosis - just clinical OR direct laryngoscopy
Tx - keep upright after feeds, acid reducers if reflux
**Reassurance - Most will spontaneously resolve by 18mos!!
Vitamin deficiency that causes pellagra
Niacin (B3)
Pellagra = diarrhea + dermatitis + dementia
Thiamine (B1) deficiency causes Wernicke-Korsakoff and what other pathology?
Beriberi
Riboflavin (B2) deficiency signs (6)
- Cheilosis
- Glossitis
- Seborrheic dermatitis (on the genitals only)
- Pharyngitis
- Edema
- Erythema of the mouth
Pyridoxine (B6) deficiency signs
- Depression/irritability
- Dermatitis
- Stomatitis
- Elevated homocysteine –> venous thromboembolic dz and atherosclerosis
Four immune deficiency disorders and affect both B and T cells
Severe combined immunodeficiency (SCID)
Ataxia–telangiectasia
Hyper–IgM syndrome
Wiskott-Aldrich syndrome
SCID pathophysiology
Genetic defect (in IL-2R gamma chain or adenosine deaminase deficiency) –> failure of T cells to develop –> B cell dysfunction due to absent T cells
SCID inheritance patterns (2)
IL-2R defect = X-linked recessive (more common)
Adenosine deaminase deficiency = Autosomal recessive
Treatment for SCID
Bone marrow transplant
*the earlier the better –> hence why SCID is included in newborn screen in US
Signs of SCID
Recurrent, severe viral, fungal, opportunistic infections
Failure to thrive (low weight %ile)
Chronic diarrhea
In early infancy - eczema and bleeding (eg. post circumcision, bleeding from umbilical stump) due to thrombocytopenia
Wiskott-Aldrich syndrome
*Mutation in WAS gene –> T-cells unable to recognize actin cytoskeleton AND fewer/smaller platelets
Most common childhood systemic vasculitis–name and pathophysiology
Henoch-Schonlein purpura
IgA mediated vasculitis of the small vessels, usually after URI
Signs of Henoch-Schönlein purpura (4)
- Palpable purpura (symmetric, over her lower legs, buttocks, arms) **palpable ie we can feel the raised lesions of the purpura + its non-blanching
- Arthritis/arthralgia (most commonly knees and ankles)
- Colicky abdominal pain (due to local vasculitis)
- Renal sx if pt develops nephropathy
Tx for Henoch Schonlein purpura (mild v severe)
- Supportive = NSAIDS + hydration
2. If severe (nephrotic syndrome, HTN, acute renal failure) = hospitalize and give systemic glucocorticoids
What to use to remove foreign bodies in pre-pubertal girl (ex. toilet paper, toys) that is causing vulvovaginitis (2)
Warm water irrigation OR calcium alginite swab
Genu varum v genu valgum
Genu varum = bow-legged
Genu valgum = knock-kneed
Treatment for rickets in newborn (drug and dose)
Vitamin D repletion with 1000-2000 IU daily
Four main acute causes of hemiplegia in children
- Seizure (=Todd paralysis - postictal period); sx resolve on their own
- Hemiplegic migraine; sx resolve on their own
- Ischemic stroke (antithrombin III deficiency, PFO)
- Intracranial hemorrhage (hemophilia)
CT vs MRI, which is better at what?
CT better at showing bone (plus more easily available/faster in emergencies)
MRI better ar showing soft-tissue (plus has no ionizing radiation)
Nocturnal headaches and morning vomiting
Signs of elevated intracranial pressure!
Inc ICP worse at night bc of supine position
The inc ICP puts pressure on medullary vomiting center –> N&V
Inflammation of the larynx and trachea due to parainfluenza viral infection
CROUP = Laryngotracheitis
Clinical signs of croup (3)
Inspiratory stridor
Barky, seal-like cough
Hoarse voice
Tx of croup (mild vs severe)
Mild = stridor not happening at rest (ex. only when child cries) = oral glucocorticoids to dec edema/swelling Severe = stridor at rest/resp distress = oral glucocorticoids + nebulized epinephrine to constrict arterioles in the mucosa --> altering hydrostatic pressure --> decreases edema
Four modifiable risk factors for breast cancer
HRT
Nulliparity
Inc maternal age at first live birth
Alcohol consumption (>2 drinks/day or >7 drinks/week)
Two drugs of choice for absence seizures
Ethosuximide (Zarontin) Valproic acid (Depakote)
Clozapine only = risk of agranulocytosis. But both clozapine (Clozaril) and olanzapine (Zyprexa) are notorious for what other side effect?
Metabolic syndrome = weight gain, dyslipidemia, hyperglycemia (new onset diabetes)
–> at baseline and follow up: check BMI, fasting glucose/lipids, BP, waist circumference
What are the routine labs to measure in pt taking lithium?
Kidney (creatinine, BUN) - bc of nephrogenic diabetes insipidus & chronic interstitial nephritis
Thyroid (TSH, T4) - bc of risk of HYPOthyroidism
Main antipsychotic associated with prolonged QT at higher doses.
Ziprasidone (Geodon)
Pertussis vaccine schedule
Five doses of DTaP from 2mos-6yrs
TdaP booster in adolescence (11-18)
TdaP booster in pregnancy
Pertussis/whooping cough tx
Macrolides! (azithro, erythro, clarithro)
Give empirically even before you confirm diagnosis with bacterial culture/PCR
Difference in age of onset of Myasthenia Gravis in men v women
Women: 20s-30s
Men: 60s-80s
Patient after surgery has bilateral (or one eye worse than other) ptosis. Gets better with ice on the lids for few minutes. Pathology?
Myasthenia Gravis
Ice pack test –> slows down ACh breakdown in the synapse –> more ACh available to the few receptors still present
*still need to confirm with ACh autoantibody test
Other than the ocular signs (ptosis, diplopia), two other systems affected in myasthenia gravis?
Bulbar (dysphagia, dysarthria) Respiratory muscles (myasthenic crisis)
Tx for myasthenia gravis – medicine (1), surgical (1)?
Pyridostigimine (Achesterase inhibitor)
+/- immunotherapy (steroids, azathioprine)
Thymectomy
In pt with myasthenia gravis, why do chest CT?
To evaluate for thymoma! The autoantibodies are usually due to thymic abnormalities esp hyperplasia
Inflammation and edema of the facial nerve
Bell’s palsy
Often due to herpes simplex reactivation
Disruption of the oculosympathetic chain
Horner syndrome
- Ipsilateral ptosis
- Miosis
- Anhidrosis
Lambert-Eaton syndrome, pathophys
Autoantibodies to pre-synaptic calcium channels –> Decreased ACh release
**contrast to myasthenia gravis = autoantibodies against post synaptic ACh receptor
Lambert-Eaton highly associated with what pathology?
Small cell lung cancer (its a paraneoplastic syndrome)
Ranson criteria (5) - used to assess what path? When to assess?
Used to assess prognosis in pancreatitis. Assessed in first 48 hrs. Poor prognosis:
- Age >55
- WBC >16,000
- Glucose >200
- LDH >350
- AST >250
WBC normal value
4500-10,000
Imiquimod - class and used to tx what?
“Immune response modifier” drug
Used to treat: actinic keratosis, superficial BCC & genital warts
Pain radiates where in pancreatitis?
To the back
*plus N&V
Pain radiates where in gallbladder dzs
To the scapula
Pain radiates where in esophageal spasm?
Higher up in the chest
Pain radiates where in GERD
*trick question
Typically, there is no pain radiation in GERD
Pain radiates where in renal calculi dz?
To the groin
Murphy sign - what is it and indicative of?
Cessation of inspiratory effort on deep palpation of RUQ
Indicative of acute cholecystitis
Gnawing abdominal pain in center of upper abdomen associated with sensation of hunger
Peptic ulcer disease
PUD two top causes
#1 - H pylori infection #2 - Excessive use of NSAIDS
When to conduct an esophagogastroduodenoscopy (EGD) in a patient with suspected GERD (3) ? *since first step is usually?
First step is usually - trial with PPI, H2 receptor blocker
Do EGD if: bleeding, weight loss or dysphagia
Patient has biliary colic, + Murphy sign, plus elevated liver enzymes, amylase or lipase. Next step in workup?
ERCP to look for for choledocolithiasis
Top two causes of pancreatitis (in order)?
#1 - Gallstones! ~60% #2 - Alcohol ~30% #3 - Idiopathic 10-30%
Dyspepsia - what is it? most common etiology?
Chronic or recurrent discomfort centered in upper abdomen
- *Most commonly idiopathic!!! - no etiology found 60% of the time
- otherwise, due to PUD, GERD, gastric/pancreatic cancer
RDW (red cell distribution width) - what does it tell us?
Measures variation in red blood cell size or red blood cell volume.
–> high RDW = high variation in the size of the RBCs
Total iron binding capacity (TIBC)
Indirect measure of transferrin
Tf = transport protein for iron in serum
If “iron binding capacity” is HIGH = transferrin has lots of empty slots on it
Ferritin
Form of iron STORED in our cells
Rash that begins as pinks pots on extremities which later coalesce and become purple/purpuric
Rocky Mountain Spotted Fever
Tx for Lyme disease - early local disease vs early disseminated disease
Early local = Doxycycline or Amoxicillin 14-21 days
Early Disseminated = IV Ceftriaxone/Cefotaxime/Chloramphenicol 14-21 days
Mammogram test results categories
BI-RADS (Breast Imaging Reporting And Data System)
0 - incomplete test
1/2 - benign –> routine testing
3 - probably benign –> repeat in 6 mos
4 - suspicious for cancer –> biopsy
5 - highly suggestive of cancer –> biopsy
Tinea cruris
Jock itch
Fungal infection of the groin area
Two most common causes of small bowel obstruction
Abdominal surgery - adhesions
Hernia
Most common cause of iron deficiency anemia
Blood loss
RDW in thalessemia
Normal RDW with low MCV (microcytic)
*contrast with iron def anemia where RDW is high
Two prophylactic interventions proven to reduce number of pain crises
- Adequate hydration
2. Adequate oxygenation
Tx for Rocky Mountain Spotted Fever – non-pregnant adults/children vs pregnant women
Doxycycline (non-pregnant adults, children)
Chloramphenicol (pregnant women)
Treatment for tularemia
Streptomycin
Erythematous papules on scalp with small black bulbs (nits) at the base of the hair follicles
Head lice
Tx for head lice (first, second, third line)
First - Permethrin 1% (Elimite)
Second - Permethrin 5%
Third - Lindane 1%
Pruritic erythematous papules in between fingers, wrists, or around waist (areas where clothes fit tightly) - bite from?
Scabies (Sarcoptes scabiei)
Clusters of pruritic erythematous papules on the lower extremities (ankles, legs) - bite from?
Flea bites
Teenage boy presents with bilateral gynecomastia. Workup?
Unless you find other abnormalities (ex. small/absent testes) no need to workup further. Benign gynecomastia common in puberty –> usually resolves within 1 year
Two most common bugs implicated in acute mastitis
Strep and staph
Bug most commonly implicated in cellulitis after cat bite
Pasteurella multocida
Crescendo-decrescendo (diamond shaped) murmur
Aortic stenosis
Acute bronchitis - when to give antibiotics?
Normally do not treat uncomplicated cases with antibiotics!
Only tx if pt also has COPD or CHF, the elderly or very illl appearing
Tx for pertussis
Erythromycin 14 days OR
Azithromycin 5 days
**doesn’t alter course unless administered very early in dz
**but it does reduce transmission & hence reduces isolation time from 4 weeks to 1 week
Bug most commonly implicated in travelers diarrhea
Enterotoxigenic E. Coli
Tx for travelers diarrhea?
Fluoroquinolones (cipro, norfloxacin, ofloxacin)
Alts: TMP/SMX or azithromycin
How to differentiate btn peripheral vs central causes of vertigo (3 factors)?
Dix Hallpike maneuver
Peripheral: Vertigo reproduced after ~3-10 secs + nystagmus fixed in same direction regardless of how you turn the head + repeating maneuver lessens sx
Central (i.e. stroke): Vertigo reproduced immediately + nystagmus changes direction when you turn head + sx same even after repeating
In peripheral vestibular disorders, first line therapy?
Antihistamines (ex. meclizine)
They suppress vestibular end-organ receptors and inhibit activation of vagal response.
ANP vs BNP - where are they secreted from? Used in diagnosis of what condition?
ANP - released from atria (and partly ventricles)
BNP - released from ventricles
Both released in response to increased filling pressures/wall stress –> CHF
CHF is almost 100% unlikely if BNP level is below what value?
D-dimer sensitivity vs specificity and implication?
High sensitivity; low specificity
So mainly useful when negative! i.e. if negative, there is a very low chance patient has a DVT/PE
Drug proven to relieve dyspnea in patients with end-stage cancer
Opioids
*unknown mechanism
What four factors/signs/sx correlate significantly with diagnosis of acute bacterial cystitis
- Dysuria
- Increased frequency
- Hematuria
- Back pain (back pain isn’t exclusive to pyelo!)
Key sign seen in pyelo that you may not see in acute bacterial cystitis?
FEVER!
What four signs/sx if present/absent make you think UTI is UNLIKELY?
- No dysuria
- No back pain
- Vaginal discharge
- Vaginal irritation
When do you need to do a urine culture for a patient with suspected UTI?
If the urine dipstick or microscopic evaluation (looking for leukocytes) is negative and so the diagnosis is in question.
What do leukocyte esterase and nitrites tell us respectively when we do urinalysis for suspected UTI?
Leukocyte esterase corresponds to pyuria
Nitrites tell us presence of enterobacteria that can convert urinary nitrate to nitrite
Woman with frequent UTIs (most commonly postcoital!) - start with what behavioral changes?
Urinating/voiding right after intercourse
Acidification of urine (oral ascorbic acid/vit C, cranberry juice)
*Don’t use things like diaphragm
Prophylactic antibiotic therapy for women with recurrent UTIs (first v second v third line)?
- First line: single dose postcoital antibiotics
- Second line (if above doesn’t work): Daily single dose antibiotics for 3-6 months
- Third line (if UTIs reoccur after stopping daily dosing for 3-6 months): Daily single dose antibiotics for 1-2 years
Woman with recurrent (>4 episodes) dysuria, hematuria but negative dipsticks (other than blood), & negative urine cultures but episodes resolve with antibiotics? Should be thinking what path? What is next step in workup?
Interstitial cystitis (aka bladder pain syndrome)!
Do a cystoscopy (looking for ulcerations/fissures in bladder wall)
**tx is very complex as this can’t necessarily be cured
Male patient in his 30s-50s with urinary frequency, urgency, back pain, fever and marked pyuria. No penile discharge and he is acutely ill. Most likely etiology?
Acute prostatitis!
- We know UTIs are uncommon in men
- Urethritis (gono or non-gono) not likely to cause fever/systemic illness like this
For how long is it normal to have ear effusions after tx of AOM? What to do if it lasts longer than that duration?
Nl to have effusions up to 3 months
If longer –> refer to ENT
Tx for AOM: First line (mild vs moderate/sever) & Second Line
First line mild : amoxicillin
First line mod/severe (otalgia and/or fever >102.5F): high dose Augmentin (90mg/kg/day divided into two doses)
Second line: azithromycin
Tx for external otitis (swimmers ear) - topical or oral antibiotics?
Topical antibiotics and corticosteroids
*don’t need oral antibiotics unless refractory to topicals
Patient has bilateral LEE. Three main systems/paths we are thinking?
CHF – is there dyspnea, JVD, rales? –> get CXR then echo
Liver dz – is there ascites? –> check LFTs
Kidney dz (nephritic syndrome, ATN) – if none of the above signs –> check urinalysis
Acute Unilateral LLE –> what to do/think if (1) no trauma/signs of infection versus (2) yes, signs of inflammation/infection like erythema
If no sign of infection –> think DVT –> order doppler
If sign of inflammation/infection –> think cellulitis –> tx with antibiotics
Chronic (on/off) unilateral LEE, but no dyspnea, no trauma, no signs of inflammation –> what are we thinking? Tx?
Venous insufficiency –> Compression stockings
Most effective, proven cure for enuresis
Bed wetting alarms
*medications more effective in short term - but relapse common when discontinued
Nl bladder capacity in children (oz)
child’s age + 2 oz
Nl post void residual in bladder?
100ml
Signs of esophageal reflux in an infant (3)? Diagnosis?
Wet burps
Coughing during & after feeding
Occasional wheezing
*Diagnose with esophageal pH probe
Signs of lactose intolerance in infant (4)?
Diarrhea
Abdominal pain
Bloating
Foul-smelling stools
Signs of pyloric stenosis in infant
Projectile non-bilious vomitting
Abdominal distention
+/- palpable mass in abdomen
Simultaneous decrease in weight AND height in infant
Familial short stature
Weight decreases first, and then height (2) paths
Failure to thrive
Constitutional growth delay
Hypothyroidism - changes on growth chart (height vs weight)?
Height velocity decreases first
then the weight changes happen
Two red flag signs for severe malnutrition/failure to thrive?
Vital abnormalities:
Hypotension + bradycardia
*must be hospitalized
What happens when you give patient with mono penicillin?
They get a diffuse symmetrical rash
- this normally happens bc we misdiagnose mono as strep throat and try to tx with penicillins (amox, ampi)
- correct tx = SUPPORTIVE CARE (EBV)
Two main causes of GI bleeding in children (in order)? how to differentiate?
#1 Meckel's diverticulum (painless) #2 Intussusception (very painful)
Meckel’s diverticulum rule of 2’s (5)
Occurs in 2% of population Male to female ratio 2:1 Occurs 2 ft from ileocecal valve Usually 2in long 2% of cases have complications
Test to diagnose Meckel’s diverticulum
Nuclear technetium scan (Meckel scan)
Meckel’s diverticulum pathyophys
Congenital - Persistence of the vitelline duct
**has heterotopic epithelia = gastric & pancreatic tissue
Management of thrombosed external hemorrhoid?
Excision
- external = below dentate line
- thrombosed = hard/nodular appearance
Management of internal hemorrhoids
Rubber-band ligation
Pt with bright red blood after painful bowel movement, followed by dull ache/spasm in anal canal that resolves after several hours; no abnormalities seen on external examination
Anal fissure
*key is that the pain resolved; in thrombosed internal hemorrhoid may have pain but it would not resolve
Only calcium channel blocker proven to work in migraine prophylaxis
Verapamil
Most studied prophylactic agent for migraines
Beta blockers
Which TCA has strongest efficacy evidence for migraine prophylaxis?
Amitriptyline
Two main migraine abortives
1st line - triptans
2nd line - ergot derivatives
Cluster headaches prophylaxis (4)
- *only give the drugs during cluster!!!
1. Nifedipine (calcium channel blocker)
2. Prednisone
3. Indomethacin
4. Lithium
Mainstay treatment of cluster headaches (during attack)?
100% Oxygen via nasal cannula!
Managagement of tension-type headaches?
Trial of NSAIDs and follow up if that doesn’t work
*try to avoid opioids bc TTH is usually chronic
Painless hematuria without other sx
Bladder carcinoma
Risk factors for bladder carcinoma
Male
Smoking
Working with aromatic amines (dye, paint, aluminum, textiles, rubber)
Pseudohematuria (looks like there’s blood but there isn’t) caused by what foods (2)?
Beets
Blackberries
Food dyes
Pseudohematuria (looks like there’s blood but there isn’t) caused by what meds ?
- Chloroquine
- Metronidazole
- Phenytoin
- Rifampin
- Sulfasalazine (UC)
ASO titer
?
Two sleep aids useful for sleep ONSET problems
Zolpidem (Ambien)
Eszopiclone (Lunesta)
Sleep aid useful for sleep MAINTENANCE problems
Zaleplon (Sonata)
In Hep A, patients have prodrome flu-like illness followed by jaundice. At which stage are they most infectious?
During the prodrome
Baby born to mom with positive HBsAg. Likely to develop chronic dz or not?
When acquired early in life, the majority of those infected are likely to develop chronic disease!
Functional (urinary) incontinence
Incontinence due to a limitation that does not allow patient to void in the bathroom ex. paralysis, severe dementia ie. nothing to do with anatomy
Urge (urinary) incontinence
**most common type of incontinence in the elderly Detrusor muscle (muscle surrounding bladder) hyperactivity --> strong urge followed by involuntary loss of urine
Stress (urinary) incontinence
Loss of urine when pt has increased intra-abdominal pressure bc of weak pelvic floor muscles ex. coughing, sneezing, laughing, exercising
*women>men for obv reasons
Overflow (urinary) incontinence
Urine loss due to overdistention of the bladder
Think post-void residual > 200mL
Think BPH, neurogenic bladder (due to longstanding diabetes, alcoholism, degenerative disc dz)
Normal post-void residual
200mL is abnl
50-200mL = indeterminate
Which type of urinary incontinence is most responsive to pelvic floor strengthening (Kegel) exercises
Stress incontinence
*makes sense bc it is due to weak pelvic floor musculature
Medical management for urge incontinence (drug class + two examples)
Anticholinergics! ie prevent detrusor muscle hyperactivity!
Oxybutynin (Ditropan)
Tolterodine (Detrol)
Medical management for overflow incontinence due to BPH (two exs)
(1) Finasteride (5-alpha-reductase inhibitor) –> block DHEA to testosterone –> reduces the prostatic hyperplasia
(2) Terazosin (alpha-1 selective blocker) –> muscle relaxation
Thiazide diuretics – will cause urinary leakage, urgency or both or retention?
Urgency (and frequency) bc of increased filling
BUT NOT leakage (bc does not affect the sphincters)
Calcium channel blockers – will cause urinary leakage, urgency or both or retention?
Will cause urinary RETENTION (bc blocking contraction of detrusor muscle, PLUS the sphincters)
Alpha blockers – will cause urinary leakage, urgency or both or retention?
Leakage
BUT NOT urgency (bc the drug will cause relaxation of the sphincters; leakage throughout day so never builds up to cause urgency)
Beta blockers – will cause urinary leakage, urgency or both or retention?
Both!
*need to read up on explanation
The four hereditary hyperbilirubinemias (in order of descent through hepatocyte)
- Gilbert
- Crigler-Najjar
- Dubin-Johnson
- Rotor
Pathophys of Gilbert hyperbilirubinemia? –> unconj or conj hyperbilirubinemia?
Mildly low UDP-glucoronyltransferase –> back up –> decreased bilirubin uptake INTO the hepatocyte –> unconj hyperbili
Pathophys of Crigler-Najjar hyperbilirubinemia? –> unconj or conj hyperbilirubinemia?
ABSENT UDP-glucoronyltransferase –> NO bili conjugation –> unconj hyperbili
Pathophys of Dubin-Johnson hyperbilirubinemia? –> unconj or conj hyperbilirubinemia?
Problem getting conjugated bili OUT of the hepatocyte –> conj hyperbili
Pathophys of Rotor hyperbilirubinemia? –> unconj or conj hyperbilirubinemia?
Same as Dubin-Johnson BUT even milder
Problem getting conjugated bili OUT of the hepatocyte –> conj hyperbili
Jaundice, kernicterus, and increased unconj bili early in life
Crigler-Najjar Type I
Difference btn Type I and Type II Crigler-Najjar
Type II is less severe than Type I
Type II responds to PHENOBARBITAL (mech: increases synthesis of UDP-glucoronyltransferase in the liver)
Tx for Crigler-Najjar Type I (2)
Plasmapharesis + Phototherapy
Mostly asymptomatic or mild jaundice + increased unconj bili only with fasting or stress
Gilbert Syndrome
Grossly black liver, hyperbilirubinemia?
Dubin-Johnson
*bc the conj bili cannot be excreted –> builds up in the liver
Wilson disease –> pathophys
Problem excreting copper from hepatocytes –> [form of copper in circulation = ceruloplasmin] –> low serum ceruloplasmin + copper accumulation in the liver/brain/cornea/kidneys/joints
Signs of Wilson dz (8)
Cirrhosis Corneal deposits (Kayser-Fleischer rings) Hepatocellular Carcinoma Asterixis Hemolytic anemia Dementia Dyskinesia Dysarthris
Tx for Wilson disease (2)
Copper chelation!
Penicillamine or Trientine
G6PD deficiency –> unconj or conj hyperbili?
Unconjugated
*think back up due to intravascular hemolysis
Most common cause of conjugated hyperbili in pts
Viral hepatitis
**Accounts for 75% of jaundice in pts
Most common cause of conjugated hyperbili in pts >60yo
Extrahepatic obstruction (gallstones, pancreatic cancer)
Functional hypothalamic amenorrhea causes (4)
Anorexia
Rapid weight loss
Rigourous exercise
Significant emotional stress
Pt with amenorrhea, given Provera (medroxyprogesterone acetate) challenge 7 days, and then has period –> most likely etiology?
PCOS
Fact that patient is bleeding means they have no problems with estrogen BUT they have a problem making progesterone –> prob bc they are not ovulating = no corpus luteum to secrete progesterone
Pt with amenorrhea, initial workup negative –> progestin challenge = no withdrawal bleeding –> estrogen-progestin challenge = still no withdrawal bleeding. Most likely etiology?
Outflow tract obstruction / Anatomic defect
Signs of amphetamine withdrawal (4)
Psychomotor slowing: Hypersomnolence + Anhedonia
BUT also increased appetite + Existential crisis
Withdrawal of what drug causes hyperalert confusion
Alcohol
*overly sensitive to environmental stimuli, startled very easily
Which antidepressant has the longest half-life and therefore is less likely to cause discontinuation syndrome/withdrawal compared to the others?
Fluoxetine [Prozac] (half life = 84-144hrs)
*compare to other avg 20hrs
Pt with chronic N&V, longstanding DM2, N&V worse after eating, sometimes vomits undigested food –> etiology?
Gastroparesis
Best antiemetic for gastroparesis (name, mechanism, main adverse effect)
Metoclopramide (Reglan)
D2 receptor antagonist –> inc resting tone and contractility of gut
Adverse: Blocks dopamine –> parkisonism