Random Missed Uworld - Week 1 Flashcards

1
Q

What artery mainly supplies the pelvic organs?

A

Internal illiac artery

AKA: hypogastric artery

Other arteries branch off:

uterine arteries –> uterus

[note: ovarian a. branches from abdominal aorta]

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2
Q

What artery would supply the perinuem?

A

internal pudenal branch of the internal illiac artery

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3
Q

Acute promyeocytic leukemia (APL):

What is the chromosomal abnormality?

What does this lead to?

What is a viable treatment?

A

APL type M3 of AML, results from a t(15;17) –> PMR/RAR fusion gene, which is unable to signal for proper cellular differentiation, unlike normal retinoic acid receptor.

This could present as DIC

TX: all-trans-retinoic-acid (ATRA), which is a vitamin A derivative

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4
Q

Polymyositis

Clinical presentation

Biopsy findings

Lab findings

Related ddx

A

Clinical Presentation: progressive symmetric proximal muscle weakness

Biopsy Findings: endomysial inflammation with CD8+ T cells

Lab findings: anti-ANA, anti-Jo-1 (anti-histidyl-tRNA-synthetase), anti-Mi-2

Related ddx: dermatomyositis (like poly but with skin presentations as well - malar rash/similar to SLE)

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5
Q

SCID

severe combined immunodeficiency disorder

Etiology

Inheritance

Clinical Features

Tx:

DDX:

A

Characterized by defective T-cell development and B cell dysfunction

A genetic defect leads to failure of proper T cell development –> absence of T-cells leads to B cell dysfuction.

Inheritance could either be X-linked recessive or autosomal recessive

Recurrent infections - viral, fungal, bacterial and opportunistic! [sinusitis, otitis media, j. joveii infection…]

Failure to thrive

chronic diarrhea

tx: stem cell transpant ONLY (must be done ASAP)

DDX: congenital HIV [failure to thrive + recurrent infections - need to differentiate]

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6
Q

What is the candidal antigen skin test used for?

What are they key cells involved?

A

To determine the presence of cellular or T-cell mediated immunity through the detection of delayed-type hypersensitivity reaction (type IV)

key cells: macrophages, cytotoxic CD8+ T cells, and CD4+ helper T cells

SCID pt – anergy – no reaction

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7
Q

What are some tumors that can present psammoma bodies histologically? (5)

A

Meningioma

papillary thyroid carcinoma

mesothelioma

papillary serous CA of the ovary

papillary serous CA of the endometrium

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8
Q

Explain how the clearance of lithium could lead to its side effects seen?

What are some drug interactions?

Mgmt:

A

Acutely, lithium side effects include: GI upset (V/D) and later neurological findings (excitability, delirium) as it penetrates the CNS

Chronic toxicity, could be due to the way lithium is cleared. Lithium is mostly renally excreted thus anything that decreases glomerular filtration could lead to an increase in reabsorption at the proximal tubule (volume depletion/hyponatremia, CHF, cirrhosis)

These AEs: ataxia, fasiculations, confusion and agitaiton

Drug interactions with: thiazide diuretics, NSAIDS (not aspirin), ACE inhibitors

Mgmt: hemodyalisis for severe cases

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9
Q

Deficiency of what enzyme could lead to propionic acedemia, which presents with poor feeding, vomiting, hypotonia, lethargy, dehydration and anion gap acidosis?

Metabolism of what amino acids (4), would worsen this condition?

A

Deficiency of propionyl CoA carboxylase prevents the conversion of propionyl CoA to methylmalonyl CoA, which hten leads to propionic acedemia as it accumulates

Metabolism of valine, isoleucine, threonin, methionine results in the initial production of propionyl CoA

VOMIT = valine, odd chain FA, methionine, isoleucine, threonine.

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10
Q

What is isolated systemic hypertension and what are some causes…

A

Increased systolic BP with normal (<90) diastolic BP

This is mostly seen in the aging population due to increased arterial stiffness –> dec compliance of aorta and major peripheral arteries

Other causes: severe aortic regurg, anemia, hyperthyroidism

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11
Q

Meckel diverticulum is known as the dz of 2’s why? (5)

what is the cause?

A

Meckel’s diverticulum is a TRUE diverticulum (includes all layers not just mucosa), due to the presistence of the vitelline duct before week 9 –> vitelline cyst/omphalomesenteric duct

It is the most common congenital GI tract anomaly

Can cause: melena, RLQ pain, intussusception, volvulus, obstruction near terminal ileum

Rule of 2’s:

2 in long

2 feet from ileocecal valve

2% of population

commonly presents in the first 2 years of life

May have 2 types of epithelial (gastric / pancreatic)

-called ectopy NOT metaplasia-

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12
Q

What nerve innervates the skin of the pubic region?

A

iliohypogastric (branches off the L1 never root)

  • this nerve also innervates the anteriorlateral abdominal wall muscles and the gluteal region*
    (recall: the iliohypogastric artery supplies most of the pelvic organs)
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13
Q

Microorganisms invovled in:

Cat bites (2)

Dog bites (3)

Human bites (3)

A

Cat bites:

Pasturella multocida (mouse-like odor)

Bartonella Henselae (immunocomp host)

Dog bites:

Pasturella multocida

Strep

Staph A.

Human:

Anarobes

Strep

Eikenella Corrodens

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14
Q

What is ID50 (infectious dose) stand for?

A

The minimum number of organisms required to cause disease in 50% of the individuals

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15
Q

What is the most common form of male and female baldness?

How is it transmitted?

What is the clinical presentation?

A

Androgenetic aloplecia is the most common form of battern baldness in both males and females [reason why one of the treatments is 5-alpha reductase as it blocks the conversion to DHT]

It will present with increasing baldness, especially starting in the temporal and vertex, but the pattern and severity will depend on both circulating HORMONES and GENETICS

This condition is POLYGENIC inheritance with VARIABLE EXPRESSIVITY

Other dz that are polygenic:

androgenic aloplecia

schizophrenia

DM II

Epilepsy

HTN

glaucoma

Ischemic heart disease

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16
Q

How is cystic fibrosis diagnosed in a newborn?

What symptomatic electrolyte imbalance can this lead to?

What is a recommended supplementation?

A

It is screened for, but positive results should be confirmed with a sweat test - it will be ISOTONIC to ECF

Normally, as the sweat travels through the duct, Cl- will be absorbed, followed by Na+ and H20 –> hypotonic sweat; CF patients are not able to do this, thus their sweat would be high in sodium and chloride

–> hyponatremia (excessive loss)

RF: high temperatures, exercise

Salt supplemenation is recommended

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17
Q

What effect do alpha-adrenergic agonist have on systemic blood pressure and heart rate?

On visera?

A

alpha-adrenergic agonist increase systemic BP by stimulating adrenergic 1 receptors of the vascular walls, which –> vasoconstriction

This, effectively, will stimulate baroreceptors located in the carotid sinus and aortic arch –> reflexive vagal stimulation that will inhibit SA node, slow conudction of AV and overall DEC myocardial contractility / HR

INC cardiac afterload, INC pul cap pressure, INC LVEDP

ON visceral organs: vasoconstriction of renal and splanchnic arteries –> DEC perfusion to kidney and other visceral organs

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18
Q

What anti-hypertensive medication is recommended for heart failure patients due to their additional, independent protective factor in the prevention of deleterious cardiac remodeling? (2 categories)

A

ACE inhibitors

Angiotension II Receptor Blockers

[others: diuretics for symptomatic relief, but no long-term benefits; beta-blockers for compensated HF - contraindicated for cardiogenic shock and should be used with caution in decompensated HF]

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19
Q

What is phenytoin used for?

What is a common side effect?

What are common AEs?

A

anti-convulsive, used for grand-mal seizures, status epilepticus and partial seizures

Common side effect: gingival hyperplasia (also seen in calcium channel blockers), others include coarsing facial features and hirtuism

AEs: inteferes with folic acid, and can cause megaloblastic anemia;

contraindicated in preg, CNS manifestations such as ataxia and nystagmus,

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20
Q

Lateral epicondyle serves as the primary attachment for what muscle?

What is the function of this muscle?

What injury is frequently seen here?

A

Extensor Carpi Radialis Brevis and Extensor Digitorum

involved in wrist extension

overuse –> microtrauma –> angiofibroblastic tendonitis@ its insertion point –> lateral epicondyilitis = tennis elbow

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21
Q

What are the three major types of vaginitis:

For each - major examination findings, lab dx, tx

A

1. Bacterial Vaginosis (Gardnerella vag)

off-white, fishy order with no inflammation; clue cells, positive whiff test with KOH, >pH; tx with metronidazole or clindamycin

2. Trichomoniasis (trichomonas vaginalis)

thin yellow-green, malodorous frothy discharge w/inflammation; motile trichomonadas, >pH; tx with metronidazole and treat partner

3. Candida vaginitis (candidia albicans)

thick, cottage-cheese discharge, vag inflmmation; pseduhyphae with nl pH (3.8-4.5); tx with fluconazole

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22
Q

The method of “matching” is used in what type of studies most frequently to control what type of bias?

A

In case-control studies, matching is used to try to pair similar patients in the case group with the population of the control group. This tries to address the issue of confounding factors.

The matching factors should try to address potential confounding factors such as age, race, socioeconomic, smoking status, environmental…

an example) colorectal CA patients are the cases, and their neighbors are selected for the control, trying to match age, race, socioeconomic factors, environment; controls are choosen to match the variables of the case patients.

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23
Q

What allows for elastin’s elastic properties, especially during inspiration?

What dz impairs this property of elastin?

A

extensive cross-linking between elastin monomers, which is facilitated by lysyl oxidase

alpha-1-antitrypsin –> excessive alveolar elastin dedegration due to a protease inhibitor deficiency, thus can lead to early-onset of lower-lobe predominent emphysema

  • leads to PANACINAR emphysema
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24
Q

What makes ribosomal RNA?

Where does synthesis occur (describe this location).

What is one clinical significant of being able to visualize a nucleolus?

A

Ribosomal RNA is made by RNA POL I

Synthesis, assembly and maturation of ribosomal subunit occurs in the NUCLEOLUS

Usually, increasingly differentiated cells have a smaller nucleolus since less ribosomes are needed for protein production BUT in MALIGNANT CELLS, high metabolic activity usually have a large number of active rRNA genes and a PROMINENT NUCELOUS (basophili/dark!)

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25
Obstructive lung disease is characterized by ...(*lung volumes)* What are causes of obstructive lung disease (2): complications..
Obstruction of air flow --\> air trapping in the lungs/*airways close prematurely at high lung volumes =* INC RV DEC FVC PFTs: DEC FEV1, DEC FVC -- DEC FEV1/FVC ratio, V/Q mismatch Examples: - anatomical obstruction, such as chronic bronchitis, where hyperplasia of mucus-secreting glands in bronchi, anatomically decrease the amt of air that is able to leave the lungs * blue bloater* - DEC in lung wall elasticity, such as in emphysema, due to destruction of interalveolar wall --\> compression during expiration, and unable to breath air out * barrel-shaped chest, pink puffer*
26
Sarcoidoisis: What are hallmark clinical presentation What can be seen in imaging what can be seen in labratory
Hallmark for sarcoidosis: young, African-american female, presenting with SOB, cough, chest pain, **UVEITIS**, skin lesions, **_lofgren syndrome_** (*acute* *presentation:* **bilateral hilar adenopathy**, erythema nodosum, polyathralgia/polyarthritis) Imaging: bilateral hilar adenopathy, pulmonary reticular infiltrates Labs: **INC ACE, INC Ca2+** **_non-caseating_ granulomas (_high presence of T-lymphocytes CD4+_)**
27
What is Kartagener Syndrome? What are the consolation of clinical pres? What is its caused by?
it is a form of PRIMARY CILLIARY DYSKINESIA [**_dynein_** **arm defect affecting cilia function**] *_Clinical pres:_* **Sinus Invertus**, chronic sinusitus, bronchiectasis [due to impaired mucociliary clearance], infertility Occurs due to mutations that impairs the structure or function of cilia Inheritance is **auto recessive** via wide variety of mutations
28
What effect would hypOventilation have on PCO2?
less breathing = holding PCO2 in = INCREASED levels of PC02 more breathing = more expelling = DEC CO2 levels (ie- panic attack) If it is acute process (such as heroin overdose), then there will be uncompensated respiratory acidosis: HI PCO2, low pH (nl: 7.35-7.45), nl to mildly elevated bicarb (renal compensation requires at least 24 hours of persistent respiratory acidosis)
29
What microtubules are associted with the establishment and recurrence of hereps infection?
**Dynein**, responsible for retrograde travel (+ --\> -) helps _ESTABLISH_ infection (goes towards cell body) **Kinesin**, responsible for antegrade travel (- --\> +) helps infection _REOCCUR_, taking the virus back to the skin surface
30
What can the sensitivity and specificity of a test help you determine?
Sensitivity = how likely a person WITH a disease will test positive [*less chance of false negative, correctly identifies those with a disease*] Specificity = how likely a person WITHOUT a disease will test negative [*less chance of false positives, correctly identifies ppl without dz*] **Remember: SNOUT and SPIN** SeNsitiivty helps you rule OUT a dz SPecificity helps you rule IN a dz
31
What is the filtration fraction equation of the kidney?
**FF = GFR / RPF** Renal plasma flow could be determined from the renal blood flow via, ***RPF = (renal blood flow)\* (1-hematocrit)***
32
Expression cloning is similar to southerwestern blot; how does expression cloning function, and what types of molecules can it detect?
Both are used to detect **DNA-binding proteins** *_examples include_***: transcription factors, steroids, thyroid proteins, vitamin D receptor, retinoic acid R, DNA transcription and replication proteins, etc...** expression cloning is a type of DNA cloning, where the signal for translation and transcription are included in the clone portion; allows for the use of bacteria in the process as a mRNA is able to be made into a cDNA which then can be inserted in a plasmid, made and then identified using a DNA probe.
33
Which cytokine is needed for isotype change?
IgM --\> IgE or IgG requires **IL- 4** switch to IgA requires **IL-5** **remember: HOT T-BONE stEeAK** IL 1- fever (hot, ) IL 2- (stimulates **T** cells - helper, cytotoxic, regulatory) IL 3- stimualtes **bone** marrow growth and differentiation IL 4 - induces differentiation of TH0-TH2, promotes growth of B cells and enhances class switch to IgG and Ig**E** IL 5 - promotes differentiation of B cells. Enhances class swith to Ig**A** stimulates growth and differentiation of **e**osinophils IL 6 - stimulates aKute phase protein production, and fever
34
What are 4 drugs with low therapeutic index that we need to be careful with:
digoxin lithium theophylline warfarin *"THE WAR Does Last"*
35
What are some signs of sickle cell disease
recurrent episodes of anemia, jaudice and painful swelling of the hands and feet Autosomal Recessive inheritance
36
What causes gout and what are some of the dz etiology?
Gout is caused by tissue deposition of monosodium urate crystals Elevated uric acid levels are a known risk factor for gout -one thing that could cause **hyperuricimia**, in via increased purine metabolism **PRPP synthease** is the enzyme resposible for the activated ribose needed to make de novo synthesis of purine and pyramidine nucleotides
37
What are the structures are retroperitoneal? Which ones are secondary retroperitoneal?
***_SAD PUCKER:_*** S: suprarenal/adrenal glands A: aorta and IVC D: duodenum (2nd and 3rd part only) P: Pancreas (minus tail) U: Ureters C: Colon (desending and ascending) K: Kidneys E: Esophagus (thoracic portion) R: Rectum (partially) Secondary means that they are originally suspended in the mesentary then move to the retroperitoneal space
38
What is the equation of odds ratio?
In a standard table, it is equal to = AD/BC (attach image) Only odds ratio should be used in **case-control studies**
39
What occurs during an allergic reaction?
Anaphylactic and atopic reactions are **type I** hypersensitivity reactions. Free antigen cross links with IgE on PRE-SENSITIZED mast cells and basophils --\> cross links triggers immediate release of **vasoactive amines** that act **POSTcapillary VENULES** (histamine, etc) Reaction is RAPID due to **PREFORMED antibody IgEs** Delayed response follows due to production of arachidonic acid metabolites (leukotrinenes)
40
What are the major types of immune rejection associated with transplant? What major cell lines are involved?
**1. Hyperacute:** *within minutes* _PRE-EXISTING_ **RECPIENT *_IgG antibodies_*** react to donor antigen (type II hypersen, _activate compliment)_ **2. Acute:** * weeks - months* cellular: **CD8+ T** cells activated against donor MHCs humoral: type II hypersensitivity (ab develop against donor) **3. Chronic** *months to years* **CD4 + T** cells respond to recipeint APC presenting donor peptides, including allogenic MHC Both cellular and humoral components --\> proliferation of vascular smooth muscle and parenchymal fibrosis; dominated by arteriosclerosis **4. Graft versus host disease** *varies* GRAFTED immunocomponent _T cells proliferate_ in the immunocompromised host and reject host cells with foreign proteins
41
How can the renal excretion of a substance be determined?
Excretion = total filtration - total tubular reabsorption total filtration = GFR \* [plasma] ***inulin clearance could be used to estimate GFR*** * Creatinine could also be used BUT it will be slightly over estimated since, creatinine is moderately secreted by the renal tubules* * FF = GFRXRPF --\> GFR = RPF/FF*
42
What is the flow of CSF in the brain?
CSF is made in 4 choroid plexus found in each ventricle Choroid plexus is made of epedymal covered out growths of pia, they are fenestarted and act as teh CSF/Brain barrier Lateral ventricles, via the foramen of Monroe --\> third ventricle, then via the cerebral aqueduct of Sylvus --\> 4th ventricle --\> subarachnoid space via 3 openings (2 lateral foramen of luschka or foramen of Magendie) CSF is then returned to the venous circulation via arachnoid villi (granulations)
43
In Pellegra, Niacin is deficient --\> Dementia, diarrhea, dermatitis. How can niacin be produced endogenously?
Niacin is either obtained through dietary intake or endogenously made by **TRYPTOPHAN** **Deficient state:** In developing countries: in communities where corn is the staple food (niacin is bound and not absorable) In devloped countries: nutritional deficiency states such as alcoholics, chronic illness; also in those with **carcinoid syndrome**, prolong **isonizaid** therapy, **Hartnup dz**
44
When are erythropoeiten agents recommended to use? What is a potential side effect of their use?
They are recommended for use with anemia related to chronic kidney disease; reduce the need for blood transfusions and the complications that could lead to prolong anemia [cardiac dysfunction, weakness, mental status changes...] However, they could an **increase in the viscosity** of the blood which can lead to *_thromboembolic events*_ (vascular graft thrombosis, stroke..); also could lead to _*increase of blood pressure_*, due to possible activation of erythropoeitin receptors on the walls of vascular endothelium and smooth muscle
45
What are the 3 ddx for urinary incontience: main sx and main cause?
**1. INC stress** - loss of urethra support and inc intraabdominal pressure \> sphincter pressure --\> *_leakage with laughter, cough, sneezing, etc_* **2. Urge - detrussor overactivity** --\> sudden, overwhelming and frequent need to empty bladder **_(could be due to MS!_** *lose CNS inhibition of micturition* **3. Overflow** - impaired detrussor contractility or obstruction at bladder outlet --\> *_involuntary dribbling of urine and incomplete emptying_*
46
People with down's are at an increased risk for what 2 cancers?
**Acute myelogenous lekemia**/acute megakaryoblastic leukemia (_before 5 y/o -*m for mini*_) **Acute lymphoblastic leukemia** (usually _after 5y/o_)
47
What are some risk factors for osteoporotic bone fractures? (10)
advancing age female white, hispanic, asian (AA women have increased bone density and *thus decrease risk*!) - LOW bone density personal/family hx of fractures decreased physical activity **_low_ BMI** poor calcium and vitamin D intake *excessive alcohol and tobacco use* _premature_ menopause **glucocorticoid, anticonvulsant, anticoag, thyroid replacement meds**
48
What is first line treatment for generalized anxiety disorder?
cognitive behavioral therapy SSRI, SNRI *benzos are second line, not recommended for chronic anxiety disorder, could be used _temporarily_ while SNRI/SSRI kick in, but are contraindicated in pt with a history of substance abuse*
49
What are common signs and symptoms of primary biliary cirrhosis?
**PBC** is an **autoimmune** destruction of *_intrahepatic bile ducts and interlobules,_* typically, it is _middle aged women_, presenting with fatigue, prutitis, jaundice, (*pancreatic type of sx)* + **XANTHOMAS** increased inflammation, **granulommas** and increased **lymphocyte infiltration** **+ANA**, and many times associated with other autoimmune conditions
50
T. solium dz and presentation
Pork tapeworm **neurocyticercosis** endemic in south and central america presents with **seizures** and **cystic brain** lesions in immunocompenent patients, transmitted via i**ngestion of eggs in stool from infected individuals in infected _undercooked pork_**
51
what type of symptoms could be expected with occlusions to the middle cerebral artery?
in MCA occlusions, we could expect **CONTRALATERAL** *_hemiparesis*_ and _*hemisensory loss_* involving the _face and upper limb_ If the occlusion were to occur in the dominant hemisphere (usually left), we can possible also see *expressive and receptive aphasia due to infraction of broca's and wernike's areas*. Speech areas are usually located in the dominant side of the brain
52
Which is the polymerase that has 5' --\> 3' exonuclease activity? what is the significance of this?
**DNA polymerase I** is the _only one_ that has this ability - thus it can **descise RNA primers and replace them with DNA during DNA replication**
53
What are red neurons and when can we expect to see them after an ischemic event?
**12- 24 hours** after irreversible ischemic damage *_neurons containing:_* ***_esinophilic_* cytoplasm** **pyknotic nucleus/shrunken and basophilic** **_loss of Nissl substance_**
54
What does the normal jugular venous pulse encompass?
3 positive waves: a, c and v 2 negative waves: x and y a = right atrial contraction (absent in a. fib) c = bulging tricuspid into right atrium during right ventricular contraction/systole x = R atrial relaxation v = continued inflow of venous blood y= *passive* emptying of r. atrium after tricuspid valve opening / abrupt decrease in pressure
55
What CT findings would be suggestive of Constrictive pericarditis? The patient would show what symptoms? Causes? Contrast with hypertrophic cardiomyopathy heart on CT:
Thickening and calcification of the pericardium slow and progressive dyspnea, chronic edema and ascites On the jugular venous pressure tracing, you would get a **_rapid Y descent_ that becomes deepr and steeper with inspiration** Causes: radiation to the chest, cardiac surgery and _tuberculosis_ [*key: pt immigrating from an area TB endemic!*] Contrast with hypertrophic cardiomyopathy heart on CT: dyspnea and changes to the jugular pressure wave, **prominent a wave** - CT will not show thickening or calcification of the pericardium (could show thickening of the interventricular space) In ischemic heart disease - you might see calcifications of the coronary arteries and aorta
56
What are the biochemical change that occur in early ischemic injury?
Major early biochemical change is cessation of a_erobic glycolysis_ and _initiation of anaerobic glycolysis_...this occurs within minutes, **so almost immediately/60seconds, the affected portion of the myocardium stops contracting** --\> stunned myocardiocytes you will get depletion of ATP, and INC ADP, AMP and adenosine, INC of lactate..**adenosine** can leak out of the cell and **_act as a vasodilator to help meet demand_** ischemia **less than 30 minutes** causes **REVERSIBLE** changes, the myocardium will return to normal hours - days _Ischemia \> 30 minutes --\> IRREVERSIBLE injry_
57
What is the action of opiates, and what are some side effects?
Morphine (one type of opiate), binds mu receptors, as an agonist modulates the synpatic transmission, by **opening K+ channels and closing Ca2+ channels** --\> _decrease synaptic transmission_ ***_--\> inhibits release of Ach, NE, 5HT, glutamate and substance P_*** by acting on mu R in the gut - it could cause constipation; could also cause smooth muscle contraction at the Sphincter of Oddi --\> spasms and increase in common bile duct pressures, rarely leading to biliary colic
58
What requirement is needed to refer a patient to hospice?
survival prognosis of **\< 6 months** WITH *advanced metastatic cancers or terminal illness* requires documentation proving irreversible decline in clinical and functional status focuses on comfort and quality of life, with multidisciplinary team, within various different settings (home, nursing, specialized)
59
What is the significance of the absence of a biceps reflex?
Reflex should activate biceps brachi tendon that passes through the cubital fossa --\> activates the muscle receptors that communicate via the musculocutaneous nerve with lower motor neurons in the **anterior horn of C5-C6** **C5-C6 also control the brachioradialis reflex** **Stronger reflex?? Upper motor neuron lesion** **Absent/weak reflex?? lower motor neuron @ spinal cord**
60
What nerve groups mediate the **triceps reflex?**
C7 and C8
61
What do the follwing nerve groups innervate? C4 C5 C5,C6 C7, C8 T1
C4 - shoulder/scapula elevation C5- shoulder abduction C5,C6 - elbow flexion, wrist extension C7 - elbow extension, finger extension C8 - wrist flexion, finger flexion T1 - finger abduction
62
Acute mesenteric ischemia could lead to inadequate oxygen delivery to intestinal tissues DEC oxygen --\> affects metabolic fate of pyruvate during glycolysis; low oxygen means it can't go into TCA, why does this occur?
Usually, with oxygen, pyruvate preferentially converts to acteyl coA by **pyruvate dehydrogenase** then acetyl coA could enter the mitocondria and udnergo TCA Under **HYPOXIC** conditions, there is *intracellular accumulation of \*_**NADH\***_* --\> _inhibits pyruvate dehydrogenase_; and thus increased pyruvate --\> **LACTATE by _lactate dehydrogenase_** This allows the **regeneration of NAD+,** from NADH, which allows for *_anaerobic_* glycolysis to continue. With significant tissue ishcemia, lactate begins to accumulate in the circulation --\> lactic acidosis SX: hyperventilation (try to eliminate CO2), via induced compensatory respiratory alkalosis
63
How can one contract enterohemorrhagic E.Coli 0157:H7? Sx and complications? Mxn of pathogenesis? Distinguishing features
undercooked groud beef Could cause bloody diarrhea, and lead to hemolytic-uremic sydrome (**HUS**) Elaborates a **Shiga-Like toxin** (*_phage encoded_*) capable of inhibiting protein synthesis in colonic mucosal cells and renal endothelial cells *production _enhanced by iron deficiency_* **INACTIVATE 60S** ribosomal subunit --\> inhibition of protein synthesis and eventual cell death UNABLE to ferment SORBITOL DOES NOT PRODUCE GLUCORONIDASE Unlike enteroinvasive Ecoli, EHEC doesNOT invade intestinal mucosa Unlike enterotoxigenic E coli (ETEC), ehec does NOT produce health labile toxin or heat-stable toxin
64
Name the toxin and MXN of path: Bacillus anthracis
Anthrax **EXO**toxin --\> Edema Factor (EF) and lethal factor (LF) **Edema factor INC cyclic AMP** concentration by acting as an adenylate cycalse, causing *_edema and phagocyte dysfunction_* **Lethal factor** - **ZINC** depenent protease that inhibits mitogen activates protein kinase signaling, causing apoptosis and mutli-sys physiologic disruption
65
Name the toxin and MXN of path: Bordetella pertussis
Pertusssis toxin and Adenylate cyclase toxin Pertussis toxin: disinhibits adenyl cycalse through **G1 ADP=ribosylation, increasing cyclic AMP levels** *_causes edema and phagocyte dysfunction_* Adenylate cycalse toxin: functions as an adenylate cycalse, increasing cyclic AMP levels, causes edema and phagocyte dysfunction
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Name the toxin and MXN of path: Clostridium botulinum
Botulinum toxin **Blocks **_PRE_**synpatic release of acetylcholine** at the neuromucular junction, resulitng in *_flaccid_* paralysis
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Name the toxin and MXN of path: Clostridium difficile
Toxin A and Toxin B **Toxin A**- *_recruits and activates neutrophils_*, leading to release of cytokines that causes mucosal inflammation, fluid loss and diarrhea **Toxin B**- *_induces actin depolymerization,_* leading to mucosal cell death, bowel wall necrosis and pseudomembrane formation
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Name the toxin and MXN of path: Shingella dysenteriae
Shiga toxin *_Halts protein synthesis_* by **disabling the 60s ribosomal** subunit --\> intestinal epithelial cell death and diarrhea (bloody)
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Name the toxin and MXN of path: Streptococcus pyogenes
Pyrogenic exotoxin, Streptolysin O and S, DNAse **Pyrogenic exotoxin**- acts as a **superantigen**, inducing fever and shock. associated with scarlet fever, stretococcal toxic shock syndrome **Streptolysin O and S**- damages erythrocyte membranes, causing beta-hemolysis
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What are the functions of the different types of interferon produced during infection? (alpha, beta, gamma)
**Type I interferons (alpha and beta)** - synthesized by most human cells in response to viral infections, bind type I interferon receptors found on infected and neighobring cells and act via autocrine and paracrine signaling. --\> _transcription of antiviral enzymes_ capable of halting protein synthesis (_RNase L, endonucelase that degrades all RNA in the cell)_ and protein kinse R (incativates eIF-2, inhibiting translation intiation). _Enzymes become active ONLY in the presence of DS-RNA (_forms in the infected cell as a result of viral replication = **selectively inhibit virally infected cells** Increase expression of MHC class I on all cells and stimualte NK and cytotoxic T cells **Type II Inteferon gamma-** mainly produced by _T cells_ and _NK cells_; promoate Th1 differentiation, increases expression of *_class II MHC molecules on antigen presenting cells_*, and improves the intracellular killing ability of macrophages **[virally infected cells secrete interferon a and B NOT gamma]**
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Trisomy 18: Name the syndrome Common sx prognosis
Trisomy 18 = Edwards Syndrome complete or partical extra copy of chromosome 18, inhertited as a **meiotic nondisjunction** *error in oocyte divison occurs _prior to ovulation_ and fertilization and increases with material age \>35* **sx:** micrognathia, low-set ears, prominent occiput, **rocker bottom feet**, **clenched hands with overlapping fingers**, *(at 18 you're able to rock out!)* cardia anomalies **(ASD, VSD**), genitourinary defects (_horeshoe kidney_), gastrointestinal defects (_omphacelocele, meckel's diverticulum, malrotation_), mental retardation prenatal US findings = fetal growth restrictions Majority affected die in utero, half of life births die before age of 2 weeks, suriving pt have severe intellectual disabilties
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What are signs of gastric cancer? Metastasis to ovaries is called what? what could be seen histologically?
unintential weight loos, early satiety - signs for malignantcy + epigastric pain and gastric thickening on CT + abdominal pressure and adnexal mass suggestive of gastric and ovarian invovlement **_Krukenberg tumor_** = primary gastricCA that has metastasized to the ovary histo: nets of **signet ring cells**, appearance due to a **large amounts of mucin displacing the nucleus**
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What are circumstances in which minors do not require consent? Who are emancipated minors?
Emergency care STI, contraception substance abuse (most states) prenatal care (most states) *_Emancipated minors - do NOT need parental consent for medical treatment of any kind_* homeless, are a parent, married, military, financially independent, high school graduate
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VIPoma =? What sx could this lead to/name the syndrome
**VIPoma** is a pancreatic islet cell tumor, with excess vasoactive intestinal peptide (VIP) secretion --\> WATERY diarrhea, hypokalemia, achlorhydria syndrome [=_**WDHA syndrome**, **pancreatic chloera**_] **VIP** --\> stimulates pancreatic bicar and chloride secretion, binding to intestinal epithelial cells --\> *_adenylate cyclase activation*_ and _*increased cyclic AMP_* production, causing sodium, chloride and water secretion into the bowel (**secretory watery diarrhea** often \>3L/day) somatostain decreases production of many GI hormones; thus inhibits VIP production.
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CCK?
--\> INC of pancreatic enzymes and bicarbonate, gallbladder contraction and inhibition of gastric emptying DOES NOT cause WHDA syndrome **produced by I cells of the proximal small bowel** mucosa *_in response to fatty acids and amino acids_*
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Myasthenia gravis: what are the first symptoms What are the common underlying etiologies
muscle weakness, *_with extraocular muscles most commonly affected_*; pt often experience ptosis and diplopia -- muscle weakness _worsens with activity_ and pt often note that their _sx are worse at the end of the day_ Most have found to have a **thymoma** or **thymic hyperplasia** [thymus is derived from the _THIRD PHARYGEAL POUCH_ as are the inferior parathyroid gland]
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What is the structure of a case-control study? What is typically measured?
People with diseaes of interest (cases) and people without the disease (control) asked about previous exposure to the varibale being studied. The main measure of association is the **exposure odds ratio = what is the odd for someone to have the disease with expsoure vs without exposure**
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What are gram negative rods that are non-lactose fermenters?
Shigella (no H2S production ) Salmonella and proteus (H2s production) Pesudomonas aerugionos (ox positive) ***"Shig, Sal, and Ari protest lactose"***
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E coli and Enterobactr cloaecae are both common causes of UTI in women, what is one distinguishing feature?
Both are gram negative rods that are fast fermenters of lactose (pink colonies) One distinguishing feature is that E. Coli **indole positive =** ability to covert *_tryptophan to indole_*
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All pancreatic enzymes (except amylase and lipase) are synthesized and secreted in an incative form to protect the pancreas from autodigestion (*zymogens*) what are some protective mechanisms in place to limit the amount of trypsinogen that becomes prematurely activates If this is disrupted, what could this lead to?
Trypsinogen --\> trypsin (via duodenal enterokinase) --\> activate all the other proenzymes and other trypsinogens thus a small amount of activated trypsin can result in an activation cascade **Serine peptidase inhibitor Kazal type 1 (Spink1)** trypsin itself can be its own inhibitor by cleaving other trypsin molecules and rendering them inactive = critical to prevent large amounts of trypsin from forming within pancreatic tissue --\> pancreatitis! *hereditary pancreatitis is a rare disorder that results from mutations invovling the _trypsinogen or SPINK1 genes_ --\> pancreatic autodigestion*