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MMW1p2

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ibench85lbs's version from 2016-07-18 02:33

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From [obinno59.2-two's 4; Quick review 3]:
Question Answer
AAldose reductase
EFructose
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From Quick review 2 (obinno59's private):
Question Answer Column 3
PUSPneumonia(atypical), URI's, STDsMaCroLides treat PUS, EZ to C = , = azithro,clarithro, erythromycin(Got a atypical problem? Call an ACE) used for pneumonia (mycoplasma, chlamydia, legionella)
VACUuM THe Bed Room(Vibrio C., Acne, Chlamydia, Ureaplama U., Mycoplasma, Borrelia, Rickettsia, TularemiaTETRACYCLINE
HENS PEcK(H. flu, Enterbacter, Neisseria, Serratia, Proteus, E. coli, Klebsiella, gram + cocci)1st &2nd gen cephalosporin
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From Quick review 1 (obinno59's private):
Question Answer
EF-1,6-BPase
GF-2,6-BP
HPFK-1
JPFK-2
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From [obinno59.2-two's 4; Quick review 3]:
Question Answer Column 3
33 y/o W has increasing dyspnea and productive gelatinous sputum. Afrebile, AB is directed towards what to cause her illness?A)Alpha-antitrypsin
B)DNA top I
C)GM-CSF
D) Neutrophilic myeloperoxidase
-The pt has Pulm alveolar proteinosis( PAP): AB against GM-CSF

-GM-CSF: stimulates Macrophages to breakdown and get rid of excess surfactant

- PAP is usally AI but can be congen.

-PAP: impaired surfactant clearance(accum) by alveolar macrophages. Can be primary or secondary to leukemia.

-DNA Top I: Seen in Scleroderma; a/w fibrosis

-Alpha-antitrypsin: Panacinar emphysema

--Neutrophilic myeloperoxidase: C- ANCytoA= Wegners granulomatosis
If a child swallows a peanut yesterday now he is febrile, hypotensive, increased tympany on percussion over Lower lung posteriorily,hemicircular area of density on CT scan, what is the ML complication?Lab: Hb= 13, WBC= 6K-Resorption atelectasis
-Bronchiectasis
-Bronchopneumonia
-Lung abscess
The kid has a complete obstruction of a bronchus. Given the time-frame he is ML to develop.: resorption of air and localized atelectasis

-Bronchiectasis: takes weeks to months

-Distal to the obstruction: Bronchopneumonai and abscesses could form, but leukocytosis would also form
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From [obinno59.2-two's 4; Quick review 3]:
Question Answer Column 3
If a pt has been working at a sandblasting environ. for years what What cell mediates this?-Mast cells
-Macrophages
-Eosinophils
The ingested sand(containing SIlica)and ingested by macrophages that secrete cytokines.
-The cytokines will recruit inflamm cells to induce fibrogenesis. Leading to Silicosis.

-Eosinophils and Mast cells are a/w HS rxn
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From [obinno59.2-two's 4; Quick review 3]:
Question Answer
What tissues convert sorbitol to fructose?(3)-Liver
-Ovaries
-Seminal vesicles
(So over Laziness)
What tissues can not convert sorbitol to fructose?(4)-Schwann cells
-Lens
-Retina
-Kidneys
Lack Sorbitol dehydrogenase
(2's lack #2 except Schwan)
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From [obinno59.2-two's 4; Quick review 3]:
Question Answer
A-Bradikinin
-Ach
-alpha-2 agonist
-histamine
-serotonin
-sheer stress
BIncrease Ca+(SHEER-STRESS)=Activates NO synthase(NOS)=converting L-arginine to citrulline= Increasing NO as well.

-Both Citrulline and NO=Vasodilators
GaGTP
HActivated Guanylyl Cyclase
INO from:
-Endothelial
-Converted L-arginine(from LPS)
OMyosin
QCalmodulin-Ca+
RcAMP
SCa+ channel blockers
T-Epinephrine
-Prostaglandin E2
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From Quick review 2 (obinno59's private):
Question Answer
Rules of 3-2's2 H ( long names) -hedgehog , homeobox

2 ( short names)- wnt , fgf

2 site of action: limbs, body whole
Hedgehog , Homeobox function-Hedgehog= base of limb patterns tat site AP axis(thorns or smoooth)
-HOMEOBOX...patterng head 2 toe(Duhh!!)=eyes , thorax suppose to be.
2 short genes(fgf, wnt) functionact @ apex of limbs:
-FGF( thnk Far Growth) responsible 4 lengthen limbs
-Wnt responsible 4 patterning @ tat site=Which side palms are on
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From Quick review 2 (obinno59's private):
Question Answer Column 3 Column 4
Fabry's(“Fab-Gal is into Ceramics”)Alpha-GAL-acto-sidase Aincr Ceramide trihexose:
-periph neuro
- angiokeratoma
-CV/renal diz
Krabbe(Blind Intelligent Intergalactic Krab)Galacto-cerebro-sidase—> incr galactocerebroside:
-blindness
-peripheral neuropathy
-developmental delay
-GLOBOIDAL cells
Niemann-Pick(Niemann Pick’s his nose with hisphinger)
(Need Phor Speed)
Sphingomyelinase—> incr Sphingomyelin: cherry macula with hepatosplenomegaly(NPS), neurodegeneration, foam cells
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From 2-two pt 2 (obinno59's private):
Question Answer Column 3
You have a 40 y/o man w/ chronic anemia, febrile, patchy infiltrates on CXR, and blood culure of streptococcus pneumoniae. He dies a few days later. On autopsy you see small, fibrotic, 5-g spleen filled w/ deposits of iron and calcium and prominent expansion of skull. Which condition probably caused this?-Sickle cell
-Beta-thalassemia
-Malaria
A)-The patient under-went auto-splenectomy. It occurs from multiple infarcts and sickling phenomenons
-Vaso-occlusive crisis affecting the lungs
-Sickle defect in β-globulin

-Beta-thalassemia could cause splenomegaly but form extramedullary hematopoiesis(like the liver)=hepatomegaly
-defects in either the α or β globin chain

-Malaria could also cause splenomegaly, but NOT autosplenectomy(fibrosis,and iron and calcium deposits)
54 y/o woman comes to u for sudden onset of HA and photophobia, fever. platelets are low, Hb is low, schistocytes are present in blood smear, Urea nitrogen and creatinine are elevated. What is the most likely cause? How could u confirm this?-DIC
-TTP
-ITP
-PNH
Blood smear: schistocytes; inidicates intravascular hemolysis...more specifically MHA

ITP and PNH will be Extravascular

DIC is also MHA but lacks the pentad. You can use elevated D-dimer levels to Dx.

TTP pentad
1)Fever
2)Transient neuro problems
3)MHA
4)ARF
5)Thrombocytopenia

In TTP, vWF is synthesised normally, initially as ULvWF but its subsequent break down (cleavage) is defective.

This is due to a lack of enzyme activity, called ADAMTS13 or vWF cleaving protease, that breaks down vWf in the blood.


TTP(vWF) is confirmed with vWF monomers in serum
A woman experiences nosebleeds, easy bruising, and bloody mense. She is febrile and hypotensive. Platelets are low and megakaryocytes are increased. PT and PTT are normal. No organomegaly What is the most likely cause?-DIC
-ITP
-TTP
-TTP and DIC would be a/w MHA: which would lead to ARF and neuro problems
-DIC= increase PT and PTT

ITP is diagnosed via an exclusion process
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From 2-two pt 2 (obinno59's private):
Question Answer Column 3
Patient's fingers turn white when exposed to cold and Coombs(direct and indirect) are pos during 4C not 37 C what cell surface substances accnt for this?-IgE
-Complement C3b
-IgG
Since Coombs is cold agglutination pos think IgM.

The IgM bind RBC and fix complement.

When the temp rises the IgM is dissociated leaving the complement on the RBC

IgE=allErgic rxns
What times are affected in a pt with Hep C?-BT
-PT
-PTT
Hep C compromises production of Factors 2,7,9,10 and Warfarin

-Warfarin is related to PT.(while PTT is related to Heparin)

-BT: measures platelet function
Patient experiences UTI then followed by Hypotention and fever.
Peripheralblood spear shows this:

Blood culture is pos for klebsiella
What is the most likely cause?
-HS
-AHA
-MHA
-The patient new sx and pos blood culture followed after uti suggest gram-neg induced endothelial damage leading to DIC

-RBC destruction is split up into two main categories (location-wise)
Extravascular and Intravascular

1)EXTRA
-HS
-AHA

2)INTRA
-MHA

The fact that we are looking at the peripheral blood spear tells us it's probably MHA
If a pt was dx w/ mucin-secreting adenocarcinoma then began to experience prolonged bleeding, ecchymoses, and fatigue what cells would be present?-Target cells
-Schistocytes
The paitents sx indicate DIC in relation with MHA
Schistocytes would be a/w with this to indicate mechanical lysis


Target cells are present during severe liver dz or Hb C dz.

HbC= substitution of a glutamic acid residue with a lysine residue. less severe sickling than sickle cell
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From 2-two pt 2 (obinno59's private):
Question Answer Column 3
What receptors are found on the heart? BV?A) alpha(1,2)
B)Beta(1,2)
C)Muscarinic(1,2,3)
-BV does not have Parasympathetic tone

1)BV=
-Alpha 1(constrict) and 2(stim causes dilation)
-Beta 2(stim by NE)= dilate
-noninnervated M3

2) Heart =
-Beta 1
-M3(stim decreases basal HR)

Bladder: alpha 1, Beta 2= prevents piss
JGC: Beta 1=renin release

M3 also: Bronchoconstrict
Beta 2: bronchodilate
Pt suffered an MI a year ago. What is the most likely complication of his disease
-Constrictive pericarditis
-Cardiac tamponande
-Systemic thromboembolism
-Constrictive pericarditis usually follows previous suppurative/ TB pericarditis(granulomatous) or 1-3 days(fibrinous)

-CT=occurs 5-7 days after acute MI

-Sysytemic thromboembolism is the MC risk given the length of time
49 y/o F has prod cough for 2 years w/ whitsh sputum. febrile, crackles, heartsounds faint and 15mm Hg inspiratory decline in systolic artial pressure. CXR =water bottle configuration. percardiocentesis=200ml of blood-TB
-G.A.S
-Staph
-Pericarditis=MC causes: TB and metastatic carcinoma

PP= CP, CT

-Water-bottle config
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From 2-two pt 2 (obinno59's private):
Question Answer Column 3
Drug of choice to treat HTN in a diabetic elderly woman w/ hyperuricemia and nephropathyA)Atenolol
B)Captopril
C)Indapamide
A) not recomm in diabetics= can blocks signs and sx of hyoglycemia

B) recomm. in diabetics with renal complications. shown
to delay renal failure(less aldosterone is called upon)

C)Is a thiazide diuretic. Not recomm in this case. Can precipitate hyperglycemia, hyperuricemia, and hyperlipidemia
What type of beta -blocker would worsen exertional angina?-Propranolol
-Nadolol
-Atenolol
-Acebutolol
-Acebutolol(also penbutalol and pindolol)(PAP)
has (ISA)= intrinsic sympathomimetic activity and thus has partial beta-1-agonist activity= so it won't cause a significant decrease in HR and O2 consump.
If you had to choose what drug-class would you use to treat Preggo-induced HTN?A)ACEI
B)Losartan
C)Methyl-dopa
D)Loops
A) and B)=No, can cause fetal-develop. problems=
-skull hypoplasia
-RF

D) No, can cause hypovolemia and (Hyper: Lipidemia, Glycemia, Uricemia)

C) Methyl-dopa is recommended along with Nifedipine and Labetalol(alpha/beta antag)
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From 2-two pt3 (obinno59's private):
Question Answer Column 3
A 15 y/o boy has a fever for 10 days and petechial rash on trunk and extremeities. Hb is NL, WBC is Low(Neutrophils are low, lymphocytes are NL) and BM shows no abnormality. What is the Dx?-ALL
-AML
-AA
-Bacterial infection
-Granulocytopenia is present, mononuclear cells are the only cells present. This could be due to N. Meningitidis infection: severe infection by Gram(-) would cause Neutrophils to move from circulation to tissue.

-NL BM excludes: AML and ALL

-In AA: BM is acellular: decrease in WBC, RBC, and platelets
Elderly pt complains of visual disturbance, dizziness, and HA, and Raynaud phenomena. Hepato/Splenomegaly is present.Russells bodies are present. What would be a finding you would see in this pt?-Monoclonal IgM spike in serum

-Bence Jones proteinuria
-Russell bodies: plasmacytoid lymphocytes w/ Ig stored in them; they have infiltrated his BM


-Russell bodies+hyperviscosity syndrome= Waldenstrom macroglobulinema(Lymphoplasmacytic lymphoma)=Monoclonal IgM spike(B-cell-lymphoma ). IgM=BIG=Viscous

-NO hepato/splenomegaly a/w MM, but monoclonal gammapathy is present(IgA &IgG). Plus in MM the cells look like NL plasma cells. Bence-Jones is seen in MM
37 y/o woman has a cough and fever for one week.
Here CBC stands out with
increased Neutrophils and metamyelocytes.Increase AP. What is the most likely Dx?`
-CML
-HCL
-ALL
-Leukimoid rxn
-Hodgkins ds, lymphocyte depletion type
-Leukocytosis+immature myeloid cells: exaggerate response to infection(leukomoid rxn) or CML

-CML: AP is NL
-Leukomoid rxn(reactive leukocytosis): AP is high;hypercell. but NL
-AP: bone formation activity


-HCL: peripheral blood leukocyte that mark w/ tartrate-resistant acid phosphatase.Under normal circumstances, TRAP is highly expressed byosteoclasts, activated macrophages, neurons

-Hodgkins: WBC does NOT increase

-ALL: ds of kids and young adults; Lymphoid cells do NOT have AP
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From Quick review 2 (obinno59's private):
Question Answer Column 3
Acute interstitial nephritis1)Drug-induced
-NSAIDS, penicillin, and diuretics
-eosinophils in urine
-can progress to renal papillary necrosis
Inflamm cells in interstitium


No significant inflamm cells(interstitium) seen in ATN
Renal papillary necrosis-Gross hematuria and flank pain
4 causes:
1)chronic analgesic abuse(phenacetin or aspirin)
2) Diabetes mellitus
3)Sickle cell trait/ds
4)Severe acute pyelonephritis
(Real Playas Need to flame up chronic)
Chronic pylonephritis1)Interstitial fibrosis and atrophy of tubules due to acute cases, vesicoureteral reflux(kids) or obstruction(adults)
2)Leads to:
-Cortical scarring w/ blunted calyces
-Thyroidization of kidneys: Atrophic tubules containing eosinophilic proteinaceous material

-Waxy cast in urine: long-standing urine stasis & RF
(Consistent pressure on CP to be Oprah)
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