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From Flashcardlet > 5/5 > Flashcards

5/5 Flashcards

1
Q

What marker can be used to monitor the risk of developing hepatocellular carcinoma in cirrhotic pts?

A

AFP (the pregnancy one)

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2
Q

What is the mode of transference of the most common type of hair loss?

A

Androgenetic Alopecia: It is a polygenic disorder with X-linked recessive inheritance pattern

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3
Q

In a hydrocele, where does the fluid collect?

A

In the tunica vaginalis, derived from the peritoneum. When it remains connected to the peritoneum, a hydrocele is created

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4
Q

What selective antibody deficiency is present in a pt who develops an anaphylactic response post blood transfusion?

A

IgA deficiency. Pt will also experience chronic otitis media and GI symptoms but otherwise be healthy and normal

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5
Q

What does squatting do to vascularity? What pt population is this important in?

A

Squatting = increases total systemic vascular resistance. in pts w/ tetralogy of Fallot, they need to increase their SVR/Peripheral VR ratio in order to decrease the right to left shunting and send blood successfully into the lungs. This will counteract arterial desaturation and cyanosis

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6
Q

What is the MOA of Cromolyn and Nedocromil?

A

They are mast cell stabilizing agents. They inhibit mast cell degranulation regardless of initial signal. Not as good as glucocorticoids, considered a secondary tx of allergic rhinitis and bronchial asthma

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7
Q

Characteristic findings of Aortic Regurgitation?

A

Bounding femoral pulses and head-bobbing (due to widened pulse pressure.) Arteries will exhibit abrupt distentions and quick collapses.

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8
Q

What are the clinical manifestations of tumor lysis syndrome and what are two treatments?

A

TLS occurs when lymphomas/leukemias are treated with chemotherapy and a large volume of cells are lysed in a short period of time. This results in a ton of potassium and uric acid build up and can lead to arrythmias or obstructive uropathy/RF.

Tx: hydration + allopurinol or rasburicase

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9
Q

What is the most common cause of bacterial meningitis in all age groups?

A

Strep pneumo. Lancet-shaped, gram positive cocci in pairs

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10
Q

What are the clinical manifestations and enzyme deficiency in Acute Intermittent Porphyria?

A

Clx: ab pain and neurologic manifestations, without photosensitivity. Urine will darken (port wine) upon standing. Urinary ALA and PBG increase.

Def: HMB synthase

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11
Q

What are the main types of eukaryotic RNA Poly and RNA? Where are they found? What toxin is associated with one of them?

Prokaryotic? What inhibits it?

A

RNA Poly I: rRNA (nucleolus) - most abundant type
RNA Poly II: mRNA (nucleoplasm) - makes proteins. Can be blocked by a-amanitin (mushroom toxin) can cause hepatotoxicity
RNA Poly III: tRNA (nucleoplasm)

Prokaryotic = one polymerase that transcribes all 3 types. Blocked by Rifampin

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12
Q

What is amyloidosis? What are AL, AA, mB2, ATTR, APP types related to?

A

Amyloidosis is the abnormal aggregation of proteins or their fragments into B-pleated sheet structures (waxy appearance)

AL: deposition of proteins from Ig Light chains (Russel bodies in multiple myeloma)
AA: Chronic diseases (RA, IBD, Ank Spond) - made of serum amyloid A
mB2: seen in end stage renal disease or dialysis pts. Can present as carpel tunnel
ATTR: heritable TTR gene mutation. Neurologic/Cardiac amyloidosis
APP: alzheimers - amyloid precursor protein

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13
Q

What is the M spike in multiple myeloma due to?

A

The production of a single type (monoclonal) Ab. This will also result in a larger kappa-lambda ratio - which is normally held at 2:1

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14
Q

What are the cytokines secreted by macs? functions?

A

IL-1: fever
IL-6: also secreted by Th2 cells
IL-8: Chemotaxis (along with C5a and LK B4)
IL-12: makes T cells become Th1 cells, also activates NK cells, upregulated when virus is present
TNF-a: Septic shock mediator, causes PMN recruitment and vascular leakage

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15
Q

What are the cytokines IL-2 and 3, and 4 and 5 do?

A

IL-2: stimulates growth of helper, cytotoxic and regulatory T cells
IL-3: Supports bone marrow cells
IL-4: enhances B cells and class switching to IgE or IgG
IL-5: enhances class switching to IgA and grows eosinophils

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16
Q

What response does a live-attenuated vaccine stimulate vs killed vaccine?

A

Live attenuated: cellular response

Killed: humoral response

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17
Q

What kind of hypersensitivity are autoantibodies?
What diseases are associated with: ANA, Anti-dsDNA, Antihistone, Anticentromere, Anti-desmoglein, Antimicrosomal, Anti SSA/B, c-ANCA, p-ANCA, antimitochondrial?

A

Type 2 Hypersensitivity
ANA - SLE - nonspecific
Anti-dsDNA - SLE (renal dz)
Anti-histone: Drug induced SLE (Hydralazine)
Anticentromere: Scleroderma
Anti-desmoglein: Pemphigus Vulgaris
Antimicrosomal: Hashimotos
Anti-SSA/B: Sjogrens
c-ANCA: Wegeners (GPA)
p-ANCA: Microscopic Polyangitis (MPA) or Churg-Strauss
antimitochondrial: Primary Biliary Sclerosis

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18
Q

What are the 4 different transplant rejections, when do they occur, and what is the pathogenesis?

A

Hyperacute: minutes; due to anti-donor Abs preformed in recipient
Acute: weeks; cell-mediated CTL’s reacting against foreign MHCs. Can tx with cyclosporine, muromonab etc
Chronic: Months-Years; class I MHCnonself is percieved by CTL’s as a MHCself w/ a foreign Ag. No tx.
Graft-vs-Host: Bone Marrow Transplant where graft T cells proliferate in the irradiated immunocompromised host and start killing “foreign” self stuff (rash, jaundice, diarrhea

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19
Q

MOA, Indication, and toxicity for Cyclosporine?

A

MOA: binds to cyclophilins and blocks differentiation and activation of T cells by inhibiting calcineurin –> no production of IL-2
Indx: suppress organ rejection after transplantation
Tox: nephrotox (tx w/ mannitol diuresis) and HTN, hirsuitism

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20
Q

MOA, Indication, and toxicity for Tacrolimus?

A

binds to FK-binding protein to inhibit calcineurin and decrease secretion of IL-2
Indx: Organ transplant recipients
Tox: Nephrotox and peripheral neuropathy

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21
Q

MOA, Indication, and toxicity for Sirolimus (rapamycin)?

A

Inhibits mTOR. Inhibits T-cell proliferation in response to IL-2
Indx: Transplantation
Tox: Hyperlipidemia, TCP, Leukopenia

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22
Q

MOA for Daclizumab?

A

IL-2 Monoclonal Ab

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23
Q

MOA, Indication, and toxicity for Azathioprine?

A

Antimetabolite/precursor of 6-mercaptopurine –> toxic to lymphocytes
Indx: transplantation, autoimmune disorders (glomerulonephritis and hemolytic anemia)
Tox: Bone marrow suppression, is metabolized by xanthine oxidase (allopurinol can increase tox)

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24
Q

MOA, Indication, and toxicity for Muromonab?

A

M-Ab to CD3 –> T-cells cant communicate or grow
Indx: Transplantation
Tox: Cytokine release syndrome –> Hypersensitivity Rxn

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25
Q

MOA, Indication, and toxicity for Mycophenolate?

A

Blocks Inosine Monophosphate DH –> prevents production of guanine –> Bs and Ts cant replicate
Indx: Transplants and SLE nephritis

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26
Q

MOA, Indication, and toxicity for Infliximab, Adalimumab, and Etanercept?

A

Blocks TNF-a

Indx: Crohns, RA, Ank Spond, Psoriasis

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27
Q

MOA, Indication, and toxicity for Rituximab?

A

ANti-CD-20 Ab –> decreases Plasma cells productivity

Indx: B-Cell non Hodgkins

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28
Q

MOA, Indication, and toxicity for Omalizumab:

A

Anti-IgE antibody

Indx: Severe Asthma

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29
Q

MOA, Indication, and toxicity for Filgrastim, Sargramostim, and Aldesleukin?

A

Filgrastim and Sargramostim: IL-3 mimicers –> used in recovery of bone marrow
Aldesleukin: IL-2 mimicer –> used in renal cell carcinoma, and metastatic melanoma

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30
Q

What is paroxysmal nocturnal hemoglobinuria, and what is the cause?

A

DAF (compliment pathway) deficiency

Clx: hemosiderinuria, Fe def anemia, chronic intravascular hemolysis (jaundice), thrombosis

Dx: Ham’s test (RBC’s lyse at low pH)
Tx: ultimately will need a BM transplant, but warfarin and Fe can help

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31
Q

What is hereditary angioedema, and what is the cause?

A

C1 esterase (compliment pathway) def

Clx: increased levels of bradykinin results in hereditary angioedema

32
Q

What is erythroblastosis fetalis, and what is the cause?

A

A type II hypersensitivity rxn where maternal abs to fetal RBC Ag (usually Rh-D Abs)

If mom is Rh(-), dose anti-Rh-D IgG at 28wks and again right before delivery to protect herself from being sensitized to her 1st Rh(+) child –> every child after this will result in hemolysis of baby RBCs by mom, jaundice, hydrops fetalis

33
Q

What type of hypersensitivities are Poison ivy, and goodpastures?

A

P. Ivy = type IV

Goodpastures = Type 2

34
Q

What are some causes of eosinophilia?

A 
D: drugs
N: neoplastic stuff
A: asthma, type 1 hypers, and churg strauss
A: Allergic processes
A: Addisons disease
C: collagen vascular diseases
P: parasites (worms)
35
Q

Compare the classic complement pathway to the Alternative Pathway:

Where is compliment made?

A

Classic: IgG or IgM mediated, involves C1 to start
Alternative: microbe surface molecule mediated, involves C3 to start

Compliment is made in the liver

36
Q

What are the functions of C3b, C3a, C5a, and C5b-9?

A 
C3b = opsonization
C3a = neutrophil chemotaxis + anaphylaxis reaction
C5a = anaphylaxis reaction
C5b-9 = MAC complex
37
Q

What happens if there is a deficiency in the MAC complex?

C3 def?

A

recurrent Niessera infections (both gonn and menin)

c3 def = recurrent pyogenic sinus/RT infections (s. pneumo and h.flu) AND increased susceptability to type 3 hypers (like glomerulonephritis)

38
Q

What is the MOA and some examples of a type I Hypersensitivity reaction?

A

MOA: fast rxn. cross linking of IgE causes Mast and basophil cell degranulation–> increased histamine. skin will show wheals, and be IgE everywhere

Ex: bee stings, food allergies, hay fever, asthma, eczema, hives

39
Q

What is the MOA and some examples of a type II Hypersensitivity reaction?

A

Antibody mediated, IgG or IgM bind evil (or self) cells to cause mac responsive damage

Ex: autoimmune hemolytic anemia, pernicious anemia, ITP, Rheumatic fever, Goodpastures, bullous pemphigoid, pemphigus vulgaris

40
Q

What is the MOA and some examples of a type III Hypersensitivity reaction?

A

Immune complexes (IgG binds Ag and get stuck in tissues causing mac responsive damage)

Ex: SLE, polyarteritis nodosa, post strep glomerulonephritis, RA, serum sickness, arthus rxn (tetanus vaccine)

41
Q

What is the MOA and some examples of a type IV Hypersensitivity reaction?

A

Delayed and T cell mediated –> release lymphokines and leads to mac responsive damage. Not transferable via serum (unlike the other 3)

Ex: MS, Guillain Barre, GVH, PPD, contact dermatitis (poison ivy, nickel jewelry)

42
Q

What are the 4 main blood transfusion reactions, and what hypersensitivity are they?

A

Allergic rxn: Type I hypersensitivity against plasma proteins in transfused blood –> presents with urticaria, pruritus, wheezing, fever –> tx with antihistamines

Anaphylactic rxn: Severe. IgA def gets IgA blood –> presents with dyspnea, broncospasms, hypotension and shock

Febrile Nonhemolytic Transfusion Rxn: Type II hyper. Host Abs against donor HLA Ags/PMNs –> presents with fever, headaches, chills, flushing

Acute hemolytic transfusion Rxn: Type II hyper. w/ intravascular hemolysis (ABO incompatibility or extravascular hemolysis (host Abs attack donor RBCs.) –> presents with flank pain, fever, hypotension, jaundice (if extravascular)

43
Q

Brutons agammaglobulinemia

A

X linked, boys, No B cell maturation (due to def in a tyrosine kinase gene.) –> 6 mo old gets recurrent bacterial infections

44
Q

Selective IgA deficiency

A

Very common and doesnt usually have consequences unless getting transfused with IgA blood

45
Q

What are the signs of DiGeorge syndrome?

A

hypocalcemic (tetanys), recurrent viral/fungal infections, and congenital heart and great vessel defects, absent thymic shadow

46
Q

Hyper IgE (Jobs) Syndrome

A

Th1 cells dont make IFNy –> neutrophils cant respond to chemotactic stimuli

Clx: FATED: course Facies, cold staph Abscesses, Two rows of teeth, hi IgE, Derm problems (eczema)

47
Q

Severe combined immunodeficiency (SCID)

A

X linked, most commonly due to defective IL-2 R or an adenosine deaminase deficiency = no B’s or T’s, just NKs

Clx: Triad: failure to thrive, chronic diarrhea, thrush (dueto RSV, VZV or HSV) and no thymic shadow

48
Q

Ataxia-Telangiectasia

A

ATM gene def –> def in DNA repair enzymes

Clx: Triad: Cerebellar ataxia, spider angiomas, and IgA def. Will also see increased AFP and a risk for lymphoma/leukemia

49
Q

Wiskott-Aldrich Syndrome

A

X-linked, WASP gene mutation –> T cells cant reorganize actin cytoskeleton

Clx: WAITER: WA, immunodef, TCP (purpura), eczema, recurrent pyogenic infections

50
Q

Leukocyte adhesion deficiency

A

LFA-1 gene mutation –> defective integrin on phagocytes

Clx: recurrent bacterial/pus infections and a delayed separation of the umbilical cord

51
Q

Chediak Higashi Syndrome

A

LYST gene mutation –> microtubule failure to get phagosome and lysosome to fuse

Clx: Giant granules in the neutrophils w/ recurrent pyogenic infections by staph and strep, partial albinism, and peripheral neuropathy (siezures)

52
Q

Chronic Granulomatous disease

A

Lack of NADPH oxidase = no free radicals

Clx: Cat positive infections and a defective Nitroblue test.
Tx: TMP-SMX and IFNy

53
Q

What is the term Tropism in terms of HIV?

A

Means the preference of HIV to bind to some co-receptors on the surface of the CD4 cells. You must do a Tropism test before treating a pt with CCR5 blocker (Miravoroc)

54
Q

What is the downfall of the ELISA + Western Blot test method for HIV?

A

It can show false negatives early in the course, or false positives in babies. Use PCR test to confirm in this case

55
Q

AIDS illnesses: Histoplasma capsulatum, Bartonella Henselae, Cryptosporidium, JC virus, Cryptococcus

A

Histoplasma capsulatum: pulm symptoms only in immunocompromised (oval yeasts within macs
Bartonella Henselae: bacillary angiomatosis (cherry angiomas)
Cryptosporidium: Watery diarrhea (acid fast)
JC virus: Progressive Multifocal Leukoencephalopathy (PML)
Cryptococcus: Fungi Meningitis (india ink +)

56
Q

AIDS prophylaxis vs illnesses:

A

CD4<50 - worry about MAC - Tx with Azithromycin

57
Q

Differentiate between the 3 main types of esophagitis

A
  1. Candida: White pseudomembrane with PAS + stain for hyphate organisms
  2. HSV: punched out ulcers w/ large pink intracellular inclusions pushing nuclei to one side on histo
  3. CMV: linear ulcers with intranuclear and cytoplasmic inclusions w/ halo clearing on Histo
58
Q

What GI structures coorespond to foregut, midgut and hindgut, and what arteries supply them?

A

Foregut: down to duodenum (Celiac)
Midgut: duodenum to transverse colon (SMA)
Hindgut: distal transverse colon to rectum (IMA)

59
Q

What is the difference between a gastroschisis, and omphalocele?

A

Both are failure of lateral fold closure resulting in extrusions of abdominal contents, but gasto is NOT covered by peritoneum (and is safer) whereas an omphalocele is covered by peritoneum and causes more problems b/c includes the liver.

60
Q

What are the clinical signs of a TEF

A

TEF = tracheoesophageal fistula = blind espohageal pouch w/ fistula attached to trachea. Clx: drooling, choking, vomiting on first feeding with an air bubble in stomach on xray

61
Q

What is the difference btwn Meissners and Auerbach plexi? What disease is associated with Auerbach?

A

Meissners (Submucosal)= located in submucosal layer

Auerbach (Myenteric) = located in the muscularis externa - can result in decreased NO and thus Achalasia (bird beak)

62
Q

What is the difference between a sliding hiatal and paraesophageal hernia?

A

Sliding = most common, GE jxn is displaced upward and the stomach is an hourglass

Paraesophageal hernia = GE jxn is normal, fundus protrudes into the thorax

63
Q

What is the difference betwen a Mallory-Weiss syndrome and BoerHaave Syndrome?

A 
Mallory = alcoholics/bulimics get mucusal lacerations at GE jxn. Not transmural. Severe vomiting
BoerHaave = Transmural w/ violent retching - EMERGENCY
64
Q

What are the main electrolyte abnormalities in the following diruretics: Loop Diuretics (-mides), thiazides, acetazolamide (CA inhibitors), Amiloride (Na blockers), Spironolactone (Mc R antagonists)

A

Loops: Hypokalemia, met. alk, hypocalcemia
Thiazides: Hyponatreimia, Hypokalemia, Met alk, Hypercalcemia
CA inhibitors: Hypokalemia, Met. acid
Na blockers and Mc R antagonists: Hyperkalemia, Met. acid

65
Q

What is the MOA of a Factor Xa inhibitor?

A

An anticoagulant via blocking FXa without antithrombin activity. Will raise aPTT and PT without raising the Thrombin Time (TT)

66
Q

What will the extra and intracellular K levels be in a pt in DKA?

A

Extracellular: Increased
Intracellular: Decreased

67
Q

What should a strep pneumo vaccine target?

A

The capsule, it is s. pneumo’s #1 virulence factor

68
Q

What are the causes of gallstones during pregnancy?

A

Estrogen increases cholesterol production (HMG-CoA reductase) while Progesterone slows gallbladder motility

69
Q

What enzymes use vitamin B1 as a cofactor? What condition does this become a problem?

A

Pyruvate DH, a-Ketoglutarate DH, and Transketolase all use B1 as a cofactor.

B1 = thiamine, and is deficient in alcoholic homeless guys (wernickes)

70
Q

Which hypersensitivity are eosinophils involved in?

A

Type 2 - Antibody dependent cytotoxicity

71
Q

What is the mechanism of gallstones in Crohns pts?

A

Increased biliary acid wasting via feces (less reabsorption causes increased lithogenicity of bile. Cholesterol precipitates and forms gallstones

72
Q

What does yellow discharge from the cervical Os represent? What are you at risk for?

A

PID - caused by N. Gon or Chlamydia

Can lead to ectopic pregnancy or infertility due to scarring of fallopian tubes

73
Q

What are the side effects of the antihyperlipidemic meds: Statins, Fibrates, BABR, Niacin, Ezetimibe?

A

Statins: Hepatotox and muscle tox
Fibrates: Muscle tox (esp w/ statins) and gallstones
BABR: bloating, cramping, decreased absorption of digoxin, warfarin, fat soluble vits
Niacin: Flushing, warmth, pruritus, hepatotox
Ezetimibe: Hepatotox (w/ statins)

74
Q

What characteristics of a drug make it more likely to be metabolized by the liver?

A

Lipophilic, High Vd, good CNS penetration

75
Q

What path does anorexia present as amenorrhea?

A

Loss of pulsitile secretion of GnRH from the hypothalamus (not a a primary ovary or pituitary problem.)

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