Path Synopsis Of Missed Questions

Front 1

tertiary syphilis

Back 1

SPIROCHETENeurosyphilis (MC): meningovascular
• Vasculitis causing strokes
(2) Neurosyphilis: general paresis
• Dementia (organisms present)
Neurosyphilis: tabes dorsalis ,
***Demyelination posterior root ganglia and posterior column
(b) Ataxia
(c) Loss of vibration sensation
(d) Absent DTRs (loss of reflex arc)
(e) Argyll-Robertson pupil
• Accommodate but do react directly to light
***CSF findings-Increased protein, oligoclonal bands (demyelination), positive VDRL (cannot do RPR test on CSF), positive FTA-ABS
(4) Cardiovascular syphilis
• Aortic arch aneurysm
(5) Gummas
• Destructive lesions

Front 2

trepenema pallidium

Back 2

Characteristics
(1) Thin walled, flexible, gram negative spiral rods
(2) Cannot be cultured
(3) Transmission
• Sexual contact, vertical (transplacental)
(4) Organism produces small vessel vasculitis (endarteritis obliterans) with a plasma cell infiltrate (most vasculitides have a neutrophilic infiltrate)
(5) One-third of primary and secondary syphilis will spontaneously resolve without treatment
(6) One-third will develop latent syphilis
(7) One-third will develop tertiary syphilis
b. Primary syphilis
(1) Solitary painless (vasculitis damages nerve), indurated chancre
(2) Sites
• Shaft of the penis or the labia of a female, anus, mouth
(3) Occur 2-10 weeks after exposure and usually resolve spontaneously
c. Secondary syphilis
(1) Occurs 1-3 months after primary syphilis lesion has disappeared
(2) Contagious
(3) Maculopapular rash
(a) Commonly involves palms and soles
(b) Moist, papular lesions in genital area called condyloma lata
(4) Patchy alopecia
(5) Pericholangitis
• Increased alkaline phosphatase but no cholestasis
(6) Nephrotic syndrome
• Membranous glomerulopathy
(7) Generalized lymphadenopathy (85%)
(8) Meningitis
d. Latent syphilis .
(1) No lesions present
• Serologic tests remain positive and continuing infection is present
(2) Early latent phase
(a) Lasts 1-2 yrs after secondary syphilis
(b) Symptoms of secondary syphilis can reappear and infect others
(3) Late latent phase
(a) Can last many years
(b) Not infective
e. Tertiary syphilis
(1) Neurosyphilis (MC): meningovascular
• Vasculitis causing strokes
(2) Neurosyphilis: general paresis
• Dementia (organisms present)
(3) Neurosyphilis: tabes dorsalis
(a) Demyelination posterior root ganglia and posterior column
(b) Ataxia
(c) Loss of vibration sensation
(d) Absent DTRs (loss of reflex arc)
(e) Argyll-Robertson pupil
• Accommodate but do react directly to light
(f) CSF findings
• Increased protein, oligoclonal bands (demyelination), positive VDRL (cannot do RPR test on CSF), positive FTA-ABS
(4) Cardiovascular syphilis
• Aortic arch aneurysm
(5) Gummas
• Destructive lesions
f. Congenital syphilis
(1) Transplacental
• After the third month of pregnancy
(2) Signs and symptoms at birth or later during the first year of life
(3) Early signs
(a) Saber shins
• Due to periostitis
(b) Saddle nose deformity
• Due to destruction of the nasal cartilage
(c) Rhagades
• Fissuring of the skin around the mouth and nose that heals with long, thin scars
(4) Late signs
(a) Hutchinson's peg (notch) teeth
(b) Mulberry molars
(c) Sensorineural nerve deafness
(d) Interstitial keratitis of the eye
•Often leads to blindness
g. Laboratory diagnosis
(1) Dark field microscopy or direct fluorescent antibody test
• Primary or secondary syphilis
(2) Nonspecific serologic tests: detect reagin antibodies
(a) RPR and VDRL tests
(b) Reagin antibodies react with beef cardiolipin (test antigen)
(c) False positive with anti-cardiolipin antibodies (e.g., SLE)
(d) After treatment titers disappear or are low-titered
(e) False negative with antibody excess (prozone phenomenon)
• Dilute sample produces positive test
(3) Specific serologic tests
(a) FTA-ABS and hemagglutination assays
(b) Confirmatory tests
(c) Do not disappear after Rx
h. Treatment
(1) Penicillin
(2) Jarisch-Herxheimer reaction in Rx of secondary syphilis
(a) Fever, intensification of rash, flu-like symptoms
(b) Due to release of endotoxin-like substance from lysis of treponemes

Front 3

borrelia recurrentis is a ?

Back 3

spirochete

Front 4

what does borrelia recurrentis do?

Back 4

replapsing fever-->rash via a tick

Reservoirs
• Rodents
b. Transmission
(1) Tick-borne
(2) Human body louse
c. Relapses of high fever
• Due to the emergence of new antigen types
d. Hemorrhage, rash, hepatosplenomegaly, jaundice, and neurologic manifestations
e. Organisms visible in peripheral blood smears during relapses
f. Rx
• Doxycycline

Front 5

what is toxoplasmosis?

Back 5

protozoan

Front 6

toxoplasmosis

Back 6

Transmission- Ingestion of cysts in raw meat, contact with soil or cat litter, vertical transmission (transplacental)
b. Habitat-Oocysts in cat feces
c. Toxoplasmosis- Usually asymptomatic in immune competent people
Cysts containing - Tachyzoites in acute disease, Bradyzoites in chronic disease
****Encephalitis in AIDS patients
***MCC of space occupying lesion of brain in AIDS
CD4 T helper cell count < 75 cells/mm3 ,
Congenital toxoplasmosis-Pregnant women should avoid cats and eating undercooked meat, Must be infected during pregnancy to transmit to fetus
Trophozoites (tachyzoites) not cysts can pass through the placenta
Encephalitis, chorioretinitis
Leading cause of blindness in children)
Calcifications in basal ganglia, mental retardation
Rx for chorioretinitis, Pyrimethamine + sulfadiazinine + leucovorin rescue (folinic acid)

Front 7

listeria is what?

Back 7

gram + rod

Front 8

listeria

Back 8

Characteristics
a. Small gram positive rod with tumbling motility and b-hemolysis
b. Transmission
(1) Vertical transmission (transplacental or during delivery
(2) Eating contaminated, ready to eat foods; ****Soft cheeses, unpasteurized milk or cheese, hot dogs
Direct contact- Butchers, veterinarians; Immunosuppression
Major risk factor, since organisms invade mononuclear phagocytes
c. Virulence factors
(1) Actin rockets allow organism to move from cell to cell
(2) Listeriolysin O degrades cell membranes
2. Pregnancy-Abortion, premature delivery, peripartum sepsis, ***Neonatal meningitis
a. Granulomatous abscesses are noted in disseminated disease
• Granulomatis infantisepticum
b. May have delayed onset (1-4 weeks)
4. Meningitis in immunocompromised hosts
• Cancer patients and renal transplant patients
5. Rx-• Ampicillin

Front 9

what is the 3rd MCC of neonatal meningitis?

Back 9

listeria

Front 10

MCC of meningitis b/n 1mo-18 y/o is?

Back 10

neisseria menigitidis w/ nuchal rigidity and eptechia

could have sepsis w/ DIC

Front 11

what kind of bug is neisseria meningitidis?

Back 11

gram - diplococcus

Front 12

neisseria meningiitis

Back 12

Neisseria meningitidis (Slide B32)
a. Transmission
• Airborne droplets that colonize the nasopharynx
b. Site of proliferation
(1) Posterior nasopharynx
(2) About 5% of people are carriers
(3) Carrier rate increases to 35% in people living in close quarters (e.g., military recruits)
c. Virulence factors
(1) Polysaccharide capsule to resist phagocytosis by neutrophils
(2) Endotoxin (lipopolysaccharide) that can produce septic shock and DIC
(3) IgA protease that helps bacteria attach to respiratory epithelium by cleaving secretory IgA
d. Meningococcemia
(1) Predisposes to Waterhouse-Friderichsen syndrome
• Petechia expanding into ecchymoses, septic shock, DIC, bilateral adrenal hemorrhage (hemorrhagic infarction)
(2) Hematogenous spread to meninges producing meningitis
• MCC of meningitis from 1 mth to 18 yrs old
(3) Rx
• Penicillin G
(4) Rx close contacts (carriers) with rifampin (or ciprofloxacin)
(5) Polysaccharide capsule vaccine

Gram (-) diplococci
• Coffee bean appearance
b. Best grown in a CO2 rich environment on chocolate agar (Thayer Martin) at 37o
c. Polysaccharide capsule in N. meningitidis but not N. gonorrhoeae
• Inhibits phagocytosis
d. Oxidase and catalase positive
e. Identification is partially dependent on carbohydrate metabolism
(1) N. meningitides produces acid from maltose and glucose
(2) N. gonorrhoeae produces acid only on glucose
f. Fimbriae for adherence
• Important virulence factor
g. Lipopolysaccharide in cell wall
• Endotoxins
h. IgA proteases
• Cleave secretory IgA so that the Fab portion is still attached to the bacteria (helps attach organism to mucosa)
i. b-Lactamase producers
j. Tendency to disseminate if patient is deficient in C6-C9

Front 13

what does FTA-ABS test for?

Back 13

confirms spyphilis w/ no FP remains positive even after treatment of syphilis

Front 14

what is the difference b/n FTA-ABS and VLDL/RPR

Back 14

FTA-ABS remeains positive even after treatment, no FP, confirmatory test
RPR and VLDL will NOT

Front 15

rhematic fever is caused by what?

Back 15

group A strep (S. pyogenes). no speticemia b/c immunologic damage ot tissue occurs. joint pain, carditis, erythema marginatum, subq nodules, and corea may occur

Front 16

group A strep

Back 16

Transmission--Respiratory droplets
b. Most common cause of the following infections-(1) Rheumatic fever , (a) Type II and IV hypersensitivity reaction; not a septicemia
(b) Cross-reacting antibodies attack human tissue with same antigenic make-up as bacteria
(2) Post-streptococcal glomerulonephritis-Nephritic type of type III hypersensitivity reaction (immunocomplexes)
(3) Erysipelas -Spreading, raised cellulitis on skin
(4) Exudative tonsillitis due to a bacteria - Must culture or use ELISA test for streptococcal antigens, since most exudative tonsillitis is viral ; (5) Ludwig's angina- MC neck space infection
(6) Scarlet fever -Desquamating, sandpaper-like rash, strawberry tongue (tongue initially white coated before desquamation), Cellulitis with lymphangitis (“red streak”), Peritonsillar abscess, Uvula deviates to opposite side, Problem with swallowing, Necrotizing fasciitis, Streptococcal gangrene ("flesh-eating" disease)
(b) Exotoxin B
c. Common cause of the following infections-(1) Impetigo
-Close second to Staphylococcus aureus, (2) Pneumonia, (3) Meningitis, septicemia, orbital cellulitis, postpartum endometritis (puerperal sepsis), (4) Sinusitis, conjunctivitis, toxic shock syndrome, endocarditis
d. Rx-• Penicillin G or V

Front 17

tuberculoid leprosy

Back 17

Intact cellular immunity
• Produce granulomas
(2) Positive lepromin skin test (similar to PPD)
(3) Very few organisms present in lesions
(4) Hypopigmented macular skin lesions with complete sensory loss (very characteristic)
(5) Thickened superficial nerves very characteristic
(6) Autoamputation of digits
(7) Erythema nodosum absent (very characteristic)

Cannot be cultivated in culture media
b. Grows in footpad of mice and armadillos
c. Optimal growth at lower body temperatures
d. Replicates in skin, endothelial cells, Schwann cells
e. Transmission
(1) Organisms have low infectivity
(2) Prolonged contact (nasal secretions, skin lesions) with patients with lepromatous leprosy

Front 18

lepromatous leprosy

Back 18

Lack cellular immunity
• Organisms located in foamy macrophages and not in granulomas
(2) Negative lepromin skin test
(3) Numerous organisms present in lesions
(4) Multiple nodular skin lesions
• Leonine facies very characteristic
(5) Nerve involvement with patchy sensory loss
• Nerve is not palpable (very characteristic)
(6) Grenz zone (clear zone) under epidermis free of organisms
• Dermis below Grenz zone contains foamy macrophages with organisms
(7) After Rx, develop erythema nodosum leprosum (painful nodules on shins and ulna)
• Sign that cellular immunity is being restored; EN is very characteristic in lepromatous leprosy
h. Rx
(1) Dapsone + rifampin
• Danger of hemolytic anemia in patients with G6PD deficiency
(2) Thalidomide used to treat erythema nodosum leprosum

Cannot be cultivated in culture media
b. Grows in footpad of mice and armadillos
c. Optimal growth at lower body temperatures
d. Replicates in skin, endothelial cells, Schwann cells
e. Transmission
(1) Organisms have low infectivity
(2) Prolonged contact (nasal secretions, skin lesions) with patients with lepromatous leprosy

Front 19

what causes autoamputation of the digits?

Back 19

tuberculoid leprosy

Front 20

lepromin skin test is positive w/ granulomas w/o bact, hypopig skin lesions?

Back 20

tuberculoid leprosy

Front 21

causes of brain atrophy?

Back 21

atheroslcerosis, Alzherimer's and other neurodegererative dieseases
sk mm atrophy-->ALS

Front 22

waterhouse friderichsen's syndrome from?

Back 22

neisseria mengingitids gram - diplo coccus, spesis endotoxic shock and PIC. fibrin clots in adrenal glands leading to hemorrhagic infarction

Front 23

entamoeba histolytica is a what?

Back 23

protozoan

Front 24

describe entamoeba histolytica

Back 24

Transmission-• Ingestion of cysts in food, b. Amebiasis
(1) Flask shaped ulcers in the cecum-->cecal ulcers can spread otot eh liver via entering portal vein tirbutaries resulting in hepatic abscesses-->heaptic vein tributaries and spread symteically
(2) Bloody diarrhea (dysentery) without fever
***Erythrophagocytosis by trophozoites (RBCs phagocytosed)
(4) Liver abscess (trophozoites gain access to portal vein tributaries in cecum)
(a) Liquefaction of liver resembles anchovy paste
(b) Can disseminate systemically if trophozoites gain access to hepatic vein tributaries
(5) Trophozoites in diarrheal stools
(6) Cysts in non-diarrheal stools
(7) Rx
• Metronidazole

Front 25

what cuases erythrophagocytosis?

Back 25

entamoeba histolytica

Front 26

MCC of community aquaired typical pneumonia?

Back 26

strep pneumo

Front 27

strep pneumonia

Back 27

Characteristics
(1) Gram (+) lancet shaped diplococcus
(2) With increasing age, the incidence of pneumococcal infections decreases, but virulence increases
(3) Inhibited by Optochin
(4) Positive quellung reaction (capsular swelling) with addition of antiserum
(5) Presence of a capsule is most important virulence factor
(6) Transmission
• Respiratory droplets
(7) Capsular polysaccharide capsule inhibits phagocytosis
• Most important virulence factor
(8) Risks for infection
(a) Splenectomy
(b) Alcohol
(c) Sickle cell disease (dysfunctional spleen)
b. Most common cause of the following infections
(1) Community acquired pneumonia
(2) Meningitis in adults > 18 yrs old (some say N. meningitidis)
(3) Sinusitis in children
(4) Otitis media
(5) Spontaneous peritonitis in children with ascites
(6) Septicemia in splenectomized patients
(7) Septicemia causing death in children with sickle cell disease
c. Common cause of
• Otitis media (30%)
d. Rx
(1) Pneumonia: penicillin G, amoxicillin
(2) Sinusitis: amoxicillin
(3) Otitis media: amoxicillin
(4) Meningitis: ceftriaxone, cefotaxime
e. Pneumococcal vaccines
(1) Polysaccharide vaccine
• Contains 23 types of capsular polysaccharides
(2) Recommended for splenectomized individuals + penicillin
(3) Recommended for patients > 65 yrs old
(4) Polysaccharide vaccine (7 types of polysaccharide) coupled to diphtheria toxoid available for children < 2 yrs old
• Prevents bacteremic infections

Front 28

epideral hematoma

Back 28

arterial bleed of the middle meingeal artery due to temporoparietal fractures. blood on the dura

Front 29

subdural hematoma

Back 29

ruputre of brigding vein so blood collect beneath the dura

Front 30

molluscum contagiosum

Back 30

AIDS pt, raised mass w/ centra dimple like a belly button

Front 31

G6PD defient in?

Back 31

NADPH, hemolytic anemia; infections

Front 32

MPO system is dependent on?

Back 32

NADPH oxidase

Front 33

syphilitc aortitis due to?

Back 33

vasculitits of the vasa vasorum

Front 34

if a pregnant women has poor glycemic control what does that mean ot the fetus?

Back 34

high glucose in fetus, so hyperplasia of fetal islet cells

Front 35

cirrhosis and ascitis have both?

Back 35

dec plasma oncotic pressure in both fluid accumulations

Produces a transudate
b. Glinical examples of increased vascular hydrostatic pressure
(1) Pulmonan-edema in left-sided heart failure, (2) Peripheral pitting edema in right-sided heart failure (see Fig. 4-4), (3) Portal hyperlension in cirrhosis producing ascites (see Fig. FS-M)
c. Glinical examples of decreased vascular plasma oncotic pressure (hypoalhuminemia)-(1) Malnutrilion with decreased protein intake (see Fig. 7-1. left), (2) Girrhosis with decreased synthesis of albumin
(3) Nephrotic syndrome with increa.sed loss of protein in urine (>3.;ig/24 hours), (4) Malabsorption with decreased reabsorption of protein
d. Renal retention of sodium and water-(1) Increases hydrostatic pressure (increased plasma volume)
(2) Decreases oncotic pressure (dilutional effect on albiimin), (3) Kxamples—acute renal failure, glomerulonephritis

Front 36

what type of necrosis in abscesses?

Back 36

liquefactive

Front 37

what do corticosteroids do to collagen?

Back 37

they decrease collagen synthesis and dec scar tissue formation

Persistent infeclion
Most cominon cause of impaired wound healing
Stnphyloioaiis tmreus is the most commoii pathogen.
Nosocomial and community-acquired methicillin-rcsistant Stripliylaaxriis mireiis
wound infections arc increasing.
(1) Vancomycin is used for treating nosocomial infections.
(2) Trimethoprim-sull'ametlioxazole is used I'or treating comnmnity acquired infections.
2. Meiabolic disorders
• I%xanipie—diabetes meilitus increases susceptibility to infection by decreasing blootl
flow to tissue and increasing tissue levels of glucose.
3. Nmriiional deficiencies
a. Decreased protein (e.g.. malnutrition)
b. Vitamin C deficiency
c. Trace metal deficiency
(1) Copper deficiency lead.s to decreased cross-linking in collagen (also in elastic
tissue).
(2) Zinc deficiency leads to defects in removal of type 111 collagen in wound remodeling.
• Type III collagen has decreased tensile strength, which impairs wound healing.
4. Clucocorticoids
a. Interfere with collagen formation and decrease tensile strength
b. Useful clinically in preventing excessive scar formatioii
• Exaniple-dexamethasonc is used along with antibiotics to prevem scar formation in
bacterial nieningitis.

Front 38

patient swallows solvent has what happening to the hepatocytes?

Back 38

centrilobar damage w/ swelling of the cells decreased intraceulluar ATP causing dysfunctional Na/K ATPase pump and movement of sodium and water into the cells

Front 39

what are 2 types of pseudomembranous inflammation

Back 39

C. diff and corynebacterium diphtheriae

Front 40

temporal arteritis

Back 40

vessel w/ granulomatous inflammation; inc SED rate

Temporal headache, jaw claudication
(pain when chewing stretches
inflamed artery)
Blindness on ipsilaleral side
Polymyalgia rheumalica (muscle and joint
pain; normal serum creatine kinase)
Increased ESR
Treatment; corticosteroids; >50 y/o, large vessel vasculitis superficial temporal and ophthalmic artheries

Front 41

septic shock

Back 41

activates neutrophil adhesion molecules-->netropenia (more in marginating pool) caused by endotoxin

Septicemia i.s most commonly due to gram-negative pathogens (e.g., E.itlieriii/in roll).
h. Pathogenesis
(1) Endotoxins damage endothelial cells.
• Gauses the release of vasodilators such as nitric oxide and prostaglandin F
(2) Endotoxins activate the allernative complement pathway.
• Anaphylatoxins (C3a and C:ia) are produced, which stimulate mast cell release
of histamine (vasodilator)
(3) Interleukin 1 and tumor necrosis factor (TNF) arc released from macrophages,
(a) Activate neutrophil adhesion molecules, causing neutrophil adherence to
pulmonary capillaries
(b) Circulating neutrophil pool becomes part of the marginating neutrophil pool
(refer to Chapter 2).
(c) I ligh levels of TNF contribute to the vascular leakage syndrome.
• Important in the pathophysiology of acute respiratory distress syndrome
c. Pathophysiology of septic shock
(1) Initial increase in CO
• Due to rapid blood flow through dilated peripheral resistance arterioles, causing
increased return of blood to the heart
(2) Decreased FVEDP
• Due 10 neutrophil transmigiaiion ihrough the pulmonary capillaries into alveoli
producing noncardiogenic pulmonarv edema
(3) Decreased PVR
• Due to vasodilation of peripheral resistance arterioles
(4) Increased MVO,
• Tissues arc unable to extract O... because ofthe increased blood fiow.
d. Clinical findings in septic shock
(1) Warm skin, due to vasodilation of skin vessels
(2) Bounding pulse, due to increased GO
(3) Acute respiratory distress syndrome
• Due to neutrophil transmigration into alveoli
Disseminated intravascular coagulation
• Due to activation ofthe intrinsic and extrinsic coagulation system

Front 42

hypovolemic shock

Back 42

Due to excessive fluid loss (e.g.. blood, sweat)
b. Hemorrhage
(1) Foss of greater than 20% uf blood voluine (-lOOdmF) results in shock.
(2) AV/ initial effect on hemoglobin and hematocrit concentration
(a) Absolulc neulrophilie leukocytosis is the first hematologic sign.
(b) Infiision of O.W saline immediaicly uncovers the RBC deficit.
(3) Plasma i.s replaced first with fluid from the interstitial space.
• I Incovers the RBC deficit within hours to days
RBG response in the bone marrovv begins in 5 to 7 days.
c. Pathophysiology of hypovolemic shock
(1) Decreased cardiac output (CO)
• Due to decreased volume of blood
(2) Decreased left ventricular end-diastolic pressure (LVFDI1)
(3) Increased peripheral vascular resistance (PVR)
• Due to vasoconstriction of arterioles from catecholamines, ADH, and
angiotensin II. which are released in response to the decreased CO
(4) Decreased mixed venous oxygen content (MVOj)
(a) Best indicator of tissue hypoxia
(b) Measured in the right side ofthe heart vvith a Swan-Ganz catheter
(c) Indicates the degree of extraction of O. from the blood delivered to tissue
(tl) In hypovolemic shock, decreased blood flow through the microcirculation
leads to increased cxtraciion of 0 : from the blood and a decreased MVO..
d. Clinical fintlings in hypovolemic shock
(1) Gold, clammy skin due to vasoconstriction of skin vessels
(2) I Ivpotension: rapid, weak pulse (compensatory response to decreased CO)

Front 43

cardiogenic shock

Back 43

Most eominonly caused by an acute myocardial infarction
b. Pathophysiology of cardiogenic shock
(1) Decreased GO
• Due to decreased force of conlraction in the left ventricle
(2) Increased LVEDP
• Blootl aceumulales in the left ventricle.
(3) Increased PVR
• Same mechaiiism as in hvpovolemic shock
(4) Decreased MVO,
• Same mechanism as in hypovolemic shock
c. Clinical findings in cardiogenic shock
• Chest pain followed by signs similar to hypovolemic shock

Front 44

compare 3 types of shock

Back 44

septic--inc CO, dec PVR, dec LVEDP, inc MVO
hypovolemic-dec CO, inc PVR, dec LVEDP, dev MVO
cardiogenic shock dec CO, inc PVR, inc LVEDP, (b/c of b/u of blood), dec MVO

Front 45

pulmonary embolus what type of met/resp alk/acid

Back 45

resp alkalsois; dec PaO2 stim peripheral chemoreceptors inc RR and dec PaCO2 in the lungs
-other restrictive diseases sarcoid, asbestosis, asthma mild
rib fracture hypovent from pain
overstim-high alt, anxiety, estrogen, salicylate poisoning, shock, cirrhosis

Front 46

HOCM

Back 46

standing dec preload and inc the murmur
MCC of sudden death in the young
familial AD, chrom 14, missense
hypertrophy of IVS may obstruct BF below the AV-->ant leaflet of MV drawn down; aberrant myofibers in the conduction system, fatal arythmias
LV thickening
systolic ejection mumur
inc w/--standing, valsalva (inc positive intrathoracic pressure), ionotropic durgs
dec w/ BB, reclining, clenching hands squatting

i njwwj,
i think ur initial statement is incorrect... b/c Squatting actually DECREASES the systolic murmur of BOTH MVP and HCM.(squatting wont increase HCM murmurs as outflow obstruction decreases...Read on...)
With regards to what happens in Squatting...
Yes it Increases Afterload(increases vascular resistance)
but mainly, Yes it Increases Preload (more venous return), [will not decrease preload!!!]

from here on, my reply is long..as it may help those who always gets confused with such questions...

The quick way to remember, (n this is how i do it when faced with a timed exam question)....
For cases of MVP Murmur & its changes with various activites...I always ask myself.."what happens to the chordae tendinae with the given activity" n it gives me all the answers i want.
Read the following detailed explanation, understand the logic, then carry the above ques with u to any exam u face (its my version of logic, so correct me if any mistakes exsist..orelse ill go to the exam with the wrong ideas!!).

First of all..the basics:
a) Decreased preload (Valsalva, standing, hypovolemia, vasodilators etc)
b) Increased Preload (Squatting, Intravascular volume expansion, Bradycardia, Beta blockers ..etc)
c) Decrease in afterload (Hypovolemia, Nitrates....etc)
d) Increased afterload ( Squatting, Alpha stimulation, hand grip exercise, Intravascular vol expansion..etc)

Now, in Mitral Valve prolapse:
Auscultation of a pt with mitral valve prolapse reveals a Mid-systolic click, followed by a Late(ie closer to S2) systolic murmur heard best at the apex.
And in HCM:
Auscultation reveals a Systolic ejection murmur (typically is a systolic ejection crescendo-decrescendo murmur) with no clicks at all. This is best heard between the apex and left sternal border and radiates to the suprasternal notch but not to the carotid arteries or neck

The murmur of MVP (& HCM) is

1) ACCENTUATED(Accentuated for MVP means=Earlier systolic click and Longer murmur)by Decreasing Preload; eg. by standing or valsalva maneuver

The mech by which this occurs in MVP is...both valsalva maneuver and standing Decrease Venous Return to the heart thereby Decreasing Preload. This causes more laxity on the chordae tendineae which allows the mitral valve to prolapse earlier in systole, leading to an earlier systolic click (i.e. closer to S1), and a longer murmur(more time for more blood to regurgitate).
(in HCM..decreased preload increases the outflow tract obstruction)

2) DIMINSHED[ie.in MVP= Later systolic click(closer to S2) and Shorter/Lesser intensity murmur] with Increased preload (eg. Squatting, as is the case in ur doubt), .
[Hint: For MVP....the more filled the ventricle...the more its wall is stretched...the more the pull/tightness on the chordae tendinae..hence, it will be more later during the systole that the valve will be compromised n so the click will be heard later(nearer to S2), & b/c the prolapse is occuring later, this allows little blood to regurgitate into the LA thereby decreasing the murmur intensity]
[for HCM,the murmur decreases (not increases as u mentioned)..b/c this increased preload causes greater decrease in outflow tract obstruction]

So, if both MVP n HCM have same ausc findings with changes in preload, how do we diff them with auscultation??This is where Afterload comes to our rescue/or may i say worsens our lives as we have one more thing to learn.
This afterload test actually helps to diff b/w MVP and Hypertrophic cardiomyopathy/HCM as BOTH of them have a systolic murmur which Increases on standing/valsalva/decreased preload(less preload in HCM...more the obst to outflow) & viceversa with increased preload.
(note: with other systolic murmurs, a decrease in preload decreases murmur intensity, so this issue only arises to diff b/w mvp vs hcm)

So, What happens with increase in afterload...Murmur intensifies in MVP, but Decreases in HCM.
How?? By increasing the afterload (eg with a hand grip exercise)...
In MVP, the intensity of the systolic murmur increases,(note: not the timing of the systolic click) as also seen with increased preload.(this is due to the increased back pressure on the mitral valve)....
BUT in Hypertrophic cardiomyopathy, the hand grip or increased afterload decreases murmur intensity b/c obstruction in outflow tract decreases, due to greater pressure gradients which have to be overcomed across LV outflow tract to eject the blood,
(... of course the easy way to diff is that no clicks r heard in HCM, if it is mentioned in ques)

Summary...
[so, a quick summary for HCM...
if preload decreases...murmur increases
if afterload decreases...the murmur increases....
whereas if preload increases...murmur decreases, n
if afterload increases...the murmur will decrease]

{quick summary for MVP...
Decreased preload...murmur increases
Increased preload...murmur decreases
Decreased afterload...murmur decreases
Increased afterload..murmur increases}

[Also, as said earlier Aortic stenosis has a systolic murmur, but its intensity decreases when preload decreases n viceversa, unlike MVP and HCM].

i hope this helps u..Sorry, for making this too long.

Front 47

MVP

Back 47

click and murmur come lcoser to S2 when standing -->dec in PL
anxiety, valsalva
inc preload dec the murmur

Decreased preload...murmur increases
Increased preload...murmur decreases
Decreased afterload...murmur decreases
Increased afterload..murmur increases}

Front 48

inc preload dec murmur in both? what about AL?

Back 48

HOCM and MVP
inc AL dec murmor in HOCM but NOT MVP

Front 49

what causes inc/dec PL and inc/dec AL

Back 49

Decreased preload (Valsalva, standing, hypovolemia, vasodilators etc)
b) Increased Preload (Squatting, Intravascular volume expansion, Bradycardia, Beta blockers ..etc)
c) Decrease in afterload (Hypovolemia, Nitrates....etc)
d) Increased afterload ( Squatting, Alpha stimulation, hand grip exercise, Intravascular vol expansion..etc)

Front 50

what type of collagen is scar tissue?

Back 50

type 1
***scar tissue in a heart!!! esp after an AMI

Front 51

what does the murmur look like in arotic stneosis what causes aortic stneosis?

Back 51

bicuspid aortic valve
diamond shaped ejection mumur in systolie

Front 52

a transfusion rxn characterized by fever in a pt w/ neg antibody screen, neg direct coombs test and no evidence of hemoglobinuria is due to

Back 52

anti-HLA antibodies directed aginst donor leukocytes. antibodies are not detected in a regular antibody screen, which only detects antibodies aginst RBC antigens. RBCs do NOT have HLA antigens
febrile rxn-fever chills HA flushing
transplants or pregnancy

Front 53

mother is Rh- and her baby Rh- can you give her Rh?

Back 53

NO RH IG after delivery
she may have been given Rh Ig on the 28th week of her pregnancy b/c the baby turned out to be Rh- then was no need to give her any more Rh Ig
if the baby was Rh+ she would have been a cnadidate for Rh Ig to make sur that those Rh+ cells would be destroyed

Front 54

pain radiating into the left shoulder in a patient including melana w/ good PUD hx

Back 54

perforation w/ air under the diaphragm. air under the diaphragm radiates to teh shoulder.
abdominal fim sitting and lying down should be ordered

Front 55

progressive systemic sclerosis

Back 55

radial furrowing around mouth and tapered fingers w/ infarcts postive for anti-tipoisomerase antibodies

Front 56

pigmentaiton around the lips

Back 56

peutz jeghers; danger of colorectal cancer in 50%
inc sex cord tumors
polyps

Front 57

weight lifter w/ small bowel infarct

Back 57

entrapped indirect inguinal hernia

Front 58

best test for pseudomembranou scolitis

Back 58

cytotoxin assay of tool not stool gram stain

Front 59

2 things that mimic RLQ pain

Back 59

mecke's diverticulitis cannot be distinguished from acute appendicitis

Front 60

complication of sigmoid diverticular disease in diverticulitis

Back 60

inflammation not hematochezia

Front 61

intussusception in children

Back 61

blood stools mid-epigastric mass after Rotavirus vaccine

Front 62

precursor for colorectal cancer is?

Back 62

adenomatous polyp (tubular adenoma)

Front 63

what do mature RBCs make?

Back 63

glutathione in the PPP. neutralize peroxide

Lack mitochondria; therefore:
N'o citric acid cycle, No |i-oxidatioii of fatty acids, No ketone body synthesis
2. Anaerobic glycolysis-. Main source of adenosine triphosphate (A'l'P), b. I <actic acitl is the end-product of RBC! metabolism.
(1) Converted by the liver into glucose via gluconeogenesis
(2) Clucosc is utilized by RBCs for synthesizing ATP.
• This is called the Cori cycle.
3. Pentose phosphate pathway
a. Synthesizes glutathione (CSI I)
• Antioxidant that neuiralizes hydrogen peroxide (refer to Chapter 2)
b. Hydrogen peroxide is a product of oxidative metabolism,
4. Methemoglobin reductase pathway (refer to Chapter 1)
a. Methemoglobin (metl lb) refers 10 heme iron that is oxidized (Fe,v),
• MetHb eannor bind ()..
b. Reductase system converts iron to ferrous (Fe*2) so that the RBC Is can bind O,.
5. Luebering-Rapaport pathway
a. Synthesizes 2,3-BPG
b. Reijiiircd to right-shift the OBC (i.e.. release O.. to tissue; refer to (Ihapter 1)
h. Senescent RB( is
a. Phagocytosed in the cords of Billroth by splenic macrophages
b. 1 leme degradation by macrophages produces unconjugated biliriiliin.
7, Lack liuinan leukocyte antigens on their membranes (refer to Chapter 3)

Front 64

what makes NADPH?

Back 64

RBCS in the PPP
G6PD deficient hemoyltic anemia (peroxide destroys the RBC) but also a problem w/ inc infections b/c you need NADPH as a cofactor for NADPH oxidase to work in the O2 dependent MPO system

Front 65

anti-HLA antibodes destroying donor leukocytes are what?

Back 65

febrile transfusion rxn
not detected by Ab screen
not on RBCs

Front 66

MC pathogen for spontaneous peritonitis in adults w/ ascities due to cirrhosis

Back 66

E coli

Front 67

rhematic fever picture

Back 67

unifrom verrucoid sterile vegetations on mitral valve
Chorea, Arthritis, Nodules, Carditis
Erythema Marginatum, Rheumatic Fever
2 major or 1 major 1 minor
joints heart nodules subq erythema marginatum (anulare), synhams chorea
minor: criteria
inflammatory cells
temp
ESR CRP
long PR
itself
arthralgias
**cardiomegaly; throat cultures neg; strep AB, penicillin prevents RF

Front 68

keratin pearls

Back 68

SCC well differentiated
lower lip common site
upperlip and face BCC

Front 69

multiple myeloma

Back 69

plasma cells!!!! anemia pain in the ribs and back

Epidemiology
a. More common in blacks than in whites
b. Rare under 40 years of age
c. Peak incidence in 30 to 60 year olds
d. Accounts for 10% of all hematologic malignancies
e. Increased risk with radiation or benzene exposure
f. M-spike occurs in 8DSS to 90% of cases.
(1) l'sually IgG K light chain followed by IgA and pure light chain myeloma
(2) BJ represents excess light chains in urine.
(3) Urine BJ protein is positive in 60% to K0% of eases.
2. Pathophysiology
a. Chromosome abnormalities (deletions, translocations)
I). I'ossible evolution from normal plasma eells —» monoclonal gammopathy of
undetermined significance (MCUS) —> multiple myeloma
3. Pathologic findings
a. Sheets of malignant plasma cells in a bone marrow aspirate/biopsy (Fig. 13-12)
b. Plasma cells aecouni for >10% of cells in the aspirate.
4. Skeletal system findings
a. Bone pain
(1) Due to "punched out" lytic lesions (Fig. 13-13)
(a) Myeloma cells produce an inhibitor of osteoblast diflerentiation
(b) Myeloma eells release interleukin I (osteoclast activating factor)
(2) Vertebra is the most common site.
(3) Other sites include ribs, skull, pelvis.
(4) Cominonly presents with pathologic fractures
• Particularly rib lesions
b. Hypercalcemia (25% of cases)
5. Renal findings
a. Renal failure (30-30% of eases)
b. Myeloma kidney has different presentations.
(1) Proteinaceous tubular casts
(a) Composed of BJ protein
(b) BJ protein damages tubular cpilhelium
(c) liitratnbular multinucleated giant eell reaction
(2) Nephrocalcinosis
(a) Metastatic calcification of tubular basement membranes in the collecting
ducts (refer to Chapter I)
(b) Common cause of acute renal failure in niultiple myeloma
Portal hypertension associated with cirrhosis is the most common cause,
3. Clinieal findings
a. Splenomegaly
b. Peripheral blood cytopenias
• Anemia, thrombocytopenia, neutropenia alone or in combination
e. Conijiensatory reactive bone marrow hyperplasia
• Attempt by the marrow to replace lost cells
d. Correction of cytopenias vvith splenectomy

Front 70

HUS

Back 70

hemolytic uremic syndrome 0157:H7 E coli inprop cooked hamburgers; shiga toxin damage arteriole-capillar junciton of small cells platelet thrombi-->schistocytes in peripheral blood TP in bleeding time and dec plt count nl PT and PTT

Primarily occurs in children < 10 years old
Most often caused by endothelial damage at arteriole-capillary junction due to
Shiga-like loxin of Oi57,H7 serotype o f f . eoli
Organisms proliferate in undercooked beef
May also be caused by drugs and other infeclions (e.g.. Shigella, Solmonello)
Clinical Findings similar to TTP; however, CNS Findings are less frequent
Bloody diarrhea In 75% of cases
Triad: thrombocytopenia, acule renal failure, microangiopathic hemolytic anemia
Treatment: plasma exchange transfusions; corlieoslcroids
Mortality rale, 3-5%

Front 71

primary aldosteronism

Back 71

met alkalosis hypernatremia, hypokalemia high bicarb
benging tumor in the zona glomerulosa
conn's syndrome

Fpidemiology
• benign adenoma arising in the zona glomerulosa
b. Pathogenesis of electrolyte abnormalities
(1) Enhanced activity of aldosterone channels and pumps (see Fig. 4-8A)
• Increased Na' reabsorption and H* and K- excretion
(2) Increased reabsorption of Na* causes hypernatremia.
(.1) Increased excretion of K* causes hypiikaleinia.
• Hypokalemia produces severe muscle weakness (see later).
(4) Increased excretion of II* (sec Fig. 4-HH)
• Causes increased synthesis and reabsorption of HCOr (metabolic alkalosis)Effect of excess Na* in the FCF
(1) Increases plasma volume
(a) Increases stroke volume, which increases systolic blootl pressure
(b) Increases peritubular capillary hydrostatic pressure (Pu)
• Prevents the proximal tubule from reabsorbing NV
(2) Increases renal blood How
• Inhibits the renin-angiolensin-aldosteronc system causing a decrease in plasma
renin activity (PRA)
(.1) Excess Na- enters smooth muscle cells of peripheral resistance arterioles.
(a) Na- opens up Ca-'* channels causing vasoconstriction of smooth muscle
cells.
(b) Increa.sed total peripheral resistance increases the diastolic blood pressure.
d. Summary of clinical findings
(1)1 lypertension
• Due to retention of Na- (refer to Chapter 9)
(2) Polyuria and muscle weakness
• Complication of hypokalemia (see later)
(3) 1 Ivpernatremia, hvpokalemia. metabolic alkalosis
(4) Decreased PRA
(5) Absence of pitting edema and effusions
(a) Due to excessive loss of Na* in the urine from inhibition of proximal
reab.sorption of Na* (called the escape mechanism)
lb) Although THNa* is increased, the amount ol'Na--ci)niaiiiiiig lluid in the
interstitial space is //r//enough to produce pitting edema.
e. 'Ireatment is surgery,

Front 72

normal A-a gradient vs inc A-a gradient

Back 72

lungs paralysis of diaphram, depression of the resp center in the medulla (barb, brain injury); epiglottitis in HI, croup w/ parainfluenza; AML
if it is resp acidosis it is usually lung involved w/ normal A-a???
PaO2=.21 (713)-Pco2/.8
inc A-a >30...normally inc w/ age

inc A-a
vnetilation defect, perfusion defect, diffusion defect R-->L shunt (tet)

Front 73

calc A-a

Back 73

A-a=.21 (713)-co2/.8

Front 74

osteoblastic cancer

Back 74

prostate cancer inc desnity in bones, inc ALP normal GGT
mets to lower lumbar vert and pelvic bone

Front 75

primary bililar cirrhosis

Back 75

pruritis generaized bile salts in skin
obstructive jaundice w/ cirrhosis

AI destruciton of bile ducts in protal triads
antimitrochondrial antibodies and IgG inc

Ejiidemiology
a. Granulomatous destruction of bile ducts in portal triads
b. Autoimmune disorder
• Association with other autoimmime di.seases (e.g.. Sjogren's syndrome)
c. Occurs in vvomeii (>9()%) between 40 and 50 years of age
il. Progresses from a chronic inflammatory reaction to cirrhosis with PI I
c. Increased risk for hepatocellular carcinoma
2. Pathogenesis
a. ? Environmental insult affecting mitochondrial jiroteins triggering CD8 'F-cell
destruction of intralobular bile duct ei)itheliiini
Enzyme complex subunit in milochondrial niembrane is the autoantigen recognized
by CDS T cells
e. Autoantibodies (antimitochoiuirial antibodies) develop against the mitochondria
• Do //o/correlate vvitii disease activity
3. Clinical findings
a. Pruritus (20-70%)
(1) Linknown etiology {no/ bile salts in skin)
(2) Early finding well /^/yjauntlicc appears
b. Painful hejiatosplenomegalv
c. Jaundice (60%)
• Late findinf; <•////•/• most ofthe bile ducts have been destroyed
d. Inflamniatorv arthropathv (40-70%)
c. Xanthelasma (40%)
(1) Late finding
(2) Due to cholesterol in bile
f. Kayser-Fleischer ring in cornea
• Due to retention of copper
4. Laboratory findings
a. Antimiiocliondrial antibodies (AMA; >90%)
b. Serum ANA jiositive (50%)
c. Increase in serum IgM
d. Increased serum ALP and GGT
e. Increased serum cholesterol
• Component of bile
5. Treatment
a. Budesonide + ursodeoxycholic acid
b. Cholestyraniine for jiruritus
e. Liver transjilantation
• Improves survival; 70% survive 10 years

Front 76

penicillin anemia

Back 76

warm drug induced hemolytic anemia
adheres to RBC and igG Ab made aignst penicillin, macs in spleen w/ Rc for igG phagocytose the RBC and produce anemai and unconjugate dhemolytic anemia T@HS


Drug adsorption (e.g., penicillin): IgC antibody directed against the drug
attached to the RBC membrane

Front 77

systemic corticosteroids cause?

Back 77

hematologic effects: neutorphlic leukocytosis (inhibit leukocytes adhesion molecules, hence the amrginating pool becomes part of the ciculation pool of neutrophils
lymphopenia (apoptosis of B and T cells)
eosinopenia (apoptosis

Front 78

PKU

Back 78

baby exposed to phenyalanine in breast milk before th eblood level of phenyalanine inc in the baby due to def of phenylalanine hydroxyalse. can't diagnose PKU on cord lbood sample heel stick the baby before they leave the hosptial or on their first visit to teh peds

Front 79

100% parabasal cells

Back 79

menopausal no estorgen or progesterone stim of her endometrial mucosa. FSH and LH will be inc (no estorgen, no progesterone) progesterone challenge will not result in bleedin gb/c not estorgen prime mucosa

Front 80

50 y/o w/ painless mass in breast

Back 80

infiltrating ductal cancer sim to endometrial carcinoma unooppsed estrogen MCC of this cancer NOT sclerosng adenosis, fibroadenoma or cigs

Front 81

child w/ palpable flank mass and HTN + inc renin

Back 81

Wilm's tumor NOT RCC (adults). juvenile polycycstic didsease is b/l NOT unilateral and is present at birht
renal dysplasia is MC flank mass in newborn

Fpidemiology
a. .Accounts for -5% of chi ldhood cancer
b. Most common primary renal cumor in children
c. Occurs beevveen 2 and 5 years of age
d. Sporadic cype (most common)
e. Cenetic type
(1) Autosomal dominanc inhericance (ehromosomc 11)
(2) WACR syndrome
• Bllms' rumor, r/niridia (absent iris), .ycnital abnormalities, /ctardation
(3) Beckwidi-Wiedemann syntlromc
• Wilms' tumor, enlarged body organs, hemi l iypertrophy of extremities
2. Large, necrocic, gray-can cumor
a. Derived from mesonephrie mesoderm
b, Concains aborcive glomeruli and tubules, primi t ive blastemal cells, and
rhalidomyoblascs
3. Clinical findings
a. Unilaleral palpable mass in a chikl vvidi hypertension
• I lypenension tlue to renin secretion
b. Lungs are die most common site of mccascasis.
c. Wich eoinbined cherapies 2-year surv ival race is >90%,

Front 82

dermatomyositis

Back 82

heliotrope rash and rash over MCP, DIP, PIP gottron's patches
serum CK is HIGH!!! from mysitis

Front 83

hemorrhages in retina in diabetic

Back 83

rupture microaneurysms due to somotic damage to pericytes around vessels. prevneted by evaluation by opthalmologist

Front 84

reiter's syndrome

Back 84

HLA-B27, sterile conjunctivits, urethritis form Chlamydia, pain on heel at insertion of achilles and pain over dorsum of food

Front 85

biotin defiency****

Back 85

eating raw eggs
cofactor for carboxylase reactiong
pyruvate-->OAA

Front 86

MEN2a

Back 86

pheo (HTN, anxiety, drenching sweats), medullary carcionma of thyroid (calcitonin marker), hypercalcemia form parathyroid adenoma

Medullarv carcinoma, livperparathyroidism (HPTH), phcochromocvcoma

Front 87

MEN2b

Back 87

Medullary carcinoma, mucosal neuromas (lips/tongue),
phenchromocyioma
(3) l-'amilial type has a betcer prognosis

Front 88

adrenogenital syndrome

Back 88

ambigous genitalia in female due to DHT effect NOT testosterone
DHT--labia to scrotum, extends clitoris to penis

testosterone deals w/ mesonephric differentiation seminal vesciles, vas dferens, epididymis (SEED) NO effect on external genitalia

5 a reductase converts T into DHT

Front 89

wiskott aldrich syndrome

Back 89

XR, eczema, TP cellular immune defect and humoral defect (dec IGs)


Progressive deletion of B and
T cells
X-linked recessive disorder
Symplom triad: eczema, thrombocytopenia,
SP infections
Associated risk of malignant lymphoma
Defective CMI
i IgM, normal IgC, T IgA and IgE

Front 90

hypopituitarism

Back 90

non ufnctioning pit adenoma expands the sella turcica. secondary amenorrhea w/o galactorrhea, hypoglycemia dec GH and cortisol and hypothryoidism secondary type

Front 91

hypovit D

Back 91

MC due to RF b/c of loss of prox tubule 1a hydroxylase-->hypoca (tetany) w/ secondary hyperPTH low ca w/ high PTH

Front 92

hypoalbuminemia

Back 92

hypoalbuminemia dec total serum ca, noram PTH b/c free ca is normal

minimal change disease