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Cardio stuff Flashcards

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USMLE® Step 1 flashcards
1
Q

What is pulsus paradoxus?

A

Decrease in amplitude of Systolic BP > 10 mmHg on Inspiration

Seen in cardaic tamponade, asthma, OSA, pericarditis, croup

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2
Q

where is the Coronary Sinus? A Pacemaker placed in there would be used to pace??

A

Coronary sinus in the AV groove on posterior aspect of heart

used to pace Left Ventricle

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3
Q

What are the HACEK organisms? What are others that show up as culture negative endocarditis?

A

Haemophilus, Actinobacilis, cardiobacterium, eikenella, kingella

OThers for culture negative endocarditis include BArtonella, Coxiella, Mycoplasma, histoplasma, chlamydia

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4
Q

Aortic stenosis murmuer is when? Heard best where? Pulse heard? Clinical presentation?

A

Crescendo decrescendo murmur heard best almost mid systole on the Right side (aortic valve)

Loudest at heart base

PULSUS PARVUS ET TARDUS - weak and delayed peak

Can lead to SYNCOPE ANGINA DYSPNEA *SAD

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5
Q

Equation for loading dose? Maintenance Dose?

A

LD = Cp x Vd / F (Cp is target plasma concentration SS; F is oral bioavail)

MD = Cp x Cl x tau / F (tau is dosage interval)

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6
Q

Formula for half life?

A

= Vd x 0.7 / Cl

SS concentration of a drug or elimination achieved in 4-5 half lives

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7
Q

MEds associated w/ aqcuired long QT syndrome?

A

Quinidine and Sotalol

procainamide, discopyramide, ibutilide, dofetilide, and sotalol

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8
Q

what is becks triad? what does it signify?

A

Becks Triad: Hypotesnion, Distended neck veins (JVP) and muffled heart sounds

+ TAchycardia

Cardiac tamponade

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9
Q

What are the drugs that cause cutaneous flushing?

A

Vancomycin (redmans), Adenosine, Niacin, Ca channel blockers (VANC)

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10
Q

Drugs that cause a neggative chronotropic effect?

A

BB (Atenolol and Metoprolol), Non DHP CCB (Verapamil and Diltiazem), Cardiac Glycosides - Digoxin, Amiodarone and Sotalol, Cholinergic Agonists (Pilocarpine and Rivastigmine)

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11
Q

Drugs that cause myopathy

A

fibrates, niacin, hydroxychloroquine, glucocorticoids, colchicine, IFN alpha, and penicilamine

and statins duh!

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12
Q

What does digoxin do?

A

1) Blocks Na K ATPase and so increased intracellular CA and so increased contractility
2) CHOLINERGIC EFFECTS - increases Vagus parasympathetic to slow AV nodal conduction

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13
Q

Medications for CHF

A

POsitive inotropes like Digoxin, BB, ACE inhibitors and Diuretics (loops and K sparing)

K sparing - Eplerenone preferred over Amioride bc has additional effects of preventing aldosterone cardiac remodeling

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14
Q

What are problems and also mechanism of theophylline?

A

Low-moderate dose: cortical arousal and insomnia like caffeine
Acute Tox: ab pain, vomiting and diarrhea, cardiac arrhythmia and seizure (morbidity from seizure no tachyarrhythmia does not prolong QT)
Tx for Tox - GET IT OUT! Lavage and charcoal + beta blockers for arrhythmia
BZD AND BARBS 4 SEIZURES

Mechanism is inhibit PDE to increase camp and cause bronchodilators

Blocks action of adenosine

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15
Q

Terbutaline use and fx?

A

Beta agonist used to delay labor and delivery and suppress uterine contractions

FX: neonatal intraventricular hemorrhage, hypoglycemia Hypocalcemia and ileum

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16
Q

Dude what’s the alveolar gas equation?

A

Used to call PAO2

=[FiO2 x 760-47] - PaCO2 /R

=150 - PaCO2/.8

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17
Q

Diff ways to get lung abscesses

A

altered consciousness - seizures, coma, dementia, etc

immunosuppression - steroids, chronic disorders, old age, hospitalization

impaired swalling or mechanical ventilation

poor oral hygeine - dental infections and gingival disease

(VS aspiration of stomach contents which would cause chemical pneumonitis)

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18
Q

How is CFTR activate?

A

ATP-gated!!!

deletion of 3 nucleotides coding for Phe at 508 are deleted and get truncated, misfoled protein

CFTR is an ATP binding cassette transmembrane ion transporter that pumps Cl ions out of epithelial cells against a concentration gradient using ATP

Removes salt from eccrine gland duct to make sweat hypotonic normally but cant in CF

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19
Q

why do ppl w/ COPD get dyspnea during exercise? what’s that phenomenon called?

A

Dynamic Hyperinflation

hyperinflation reduces inspiratory reserve volume and limits maximal tidal volume ESPECIALLY during exercise when expiration time is limited

COPD need long time to expire and cant in exercise and so more and more air becomes trapped and then further reduction in tidal volume

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20
Q

symptoms and signs of MAC infection?

A

nonspecific: fever, weight loss, and diarrhea
+Amenia, Hepatosplenomegaly, and elevated Alk phos and Lactate Dehydrogenase levels bc reticuloendothelial system involved

Grows at high temperatures

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21
Q

Lung transplant rejection symptoms and mechanisms

A

HyperAcute - white graft rejection from ischemia

Acute - 1-2 weeks later CD8 T cells cause vascular damage and see perivascular and peribronchial lymphocytic infiltrates w/ dyspnea, dry cough and low grade fever

Chronic rejection - **inflammation of small bronchioles - Bronchiolitis Obliterans - inflammation and fibrosis narrow brionchiole
-dyspnea, nonproductive cough and WHEEZING (different than chronic in renal transplant where primarily vascular obliteration)

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22
Q

Words for silica pneomoconiosis

A

eggshell calcification of hilar nodes

birefringent silica particles surrounded by fibrous tissues

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23
Q

what does berrylyosis present as?

A

JUST LIKE SARCOIDOSIS - dyspnea and ill-defined nodular opaciticies, hilar adenopathy, non-caseating epitheliod granulomas

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24
Q

what are the acute phase reactants?

A

fibrinogen, ferritin, CRP, Serum Amyloid A, Serum Amyloid P, complement factors

Fibrinogen causes RBCs to form stacks (rouleax) that sediment at faster rate than normal RBC

Caused by release of IL1, IL6, and TNFalpha

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25
Q

what doesnt develop in Digeorge’s syndrome? What embryologic structures does it come from?

A

THIRD PHARYNGEAL POUCH –> Inf Parathyroid glands and the Thymus and Sup Parathyroid glands from 4th pharyngeal pouch

DiGeorge is abnormal 3rd and 4th puche development and abnormal Neural Crest CEll migration related to chromsome 22 deletions

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26
Q

A Study looks at how many nurses reported needle stick injury and then goes back to find out how many of them had a certain risk factor for that. Study is? Analysis w/ ?

A

Case Control Study

Odds Ratio = AD/BC

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27
Q

What is imperforate hymen?

A
  • Fully debeloped secondary sex characteristics and normal E and gonadotropins …..but absent menses in the context of normal ovarian and anterior pituitary gland function = Eugonadotropic Amenorrhea
  • 2 most frequent causes of Eugonadotropic amenorrhea are incomplete canalization of vaginal plate or mullerian duct anomalies

Imperforate hymen = incomplete canalization of vaginal plate - can get hematocolpos or accumulation of blood in vaginal canal with period leading to distention and back pain - problems pooping

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28
Q

What is the acronym for remembering valve closures on a PV loop?

A

MAAM Coco

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29
Q

Acute Pancreatitis - what enzyme is responsible?

A

TRYPSIN from trypsinogen happens within acina from acinar cell injury and leads to the activation of the other cell enzymes:

Proteases - autodigestion
Elastases - vascular damage and hemorrhage
Lipase and Phospholipase - fat necrosis

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30
Q

What does AMylase do?

A

Hydrolyzes starch to produce maltose (glu-glu), trisaccardie maltrotriose, and Limit Dextrins and does not need activation by trypsin

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31
Q

Equation for Filtration Fraction and its derivation?

A

FF = GFR/RPF

GFR = Clearance Creatinine = [U] x V / [Serum] 
RPF = Clearance PAH = [U] x V / [Serum]
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32
Q

Describe the timeline for the pathogenesis of neuronal injury w/ inadequate blood flow?

A

12-48 hours = Red Neurons (eosinophilic, pyknotic nuclei, loss of nissl)
24-72 hours = necrosis and neutrophilic infiltration

3-5 days Macrophage infiltration and phagocytosis
1-2 weeks REactive Gliosis and Vascular proliferation around necrotic area - Liquefactive necrosis w/ soft area 1 week-1 month

> 2 weeks - Glial scar and cystic area surrounded by gliosis

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33
Q

how does Acyclovir work?

A

Nucleoside analog that’s converted by viral Thymdiine Kinase into monophosphate and then cellular enzymes make is triphosphate and its incorporated into DNA –> once incorporated DNA synthesis is terminated

reduces duration of viral shedding, time for lesional healing, constitutional symptoms and llocal pain w/ first episode

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34
Q

what is locus heterogeneity? give an example

A

similar phenotype is caused by mutations in two or more different genes or loci

ex. albinism in Tyrosinease neg oculocutaneous chromosome 11 and tyrosinase pos oculocutaneous in chromosome 15

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35
Q

What the heck is citalopram?

A

SSRI just like Fluoxetine, Paroxetine, Sertraline

depression, GAD, Panic, OC, bulimia and social phobias and PSD

GI Distress and sexual dysfunction

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36
Q

Treatment for Serotonin Syndrome?

A

Cyproheptadine (5HT2 receptor antagonist)

Presents as hyperthermia, myoclonus, confusion, CV instability, flushing, diarrhea, seizures

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37
Q

what is venlafaxine?

A

SNRI - inhibits 5HT and NE reuptake

used for depression and it’s other drug Duloxetine is indicated for Diabetic Peripheral Neuropathy

Tox: increase BP, stimulant effects

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38
Q

What antidepressants would you use in Parkinsons?

A

TCAs because they have anti-cholinergic effects too which is good bc loss of Da leads to Da-Ach imabalance

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39
Q

What Neurotransmitter is important/necessary for REM sleep?

A

Ach is important for induction of REM sleep

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40
Q

Where are Lysosomal enzymes made? Function? How are they modified?

A

made in RER and then modified in golgi w/ post translational modifications that phosphorylate mannose residues and then sent to lysosomes

ICELL disease = defect in golge phosphotransferase activity and are targeted to outside of cell

normally lysosomal enzymes degrade sugar( glycosidases) and proteins (proteases)

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41
Q

What are the DNA sequences important in splicing in eukaryotic cells?

A

3’ end - AG on the intron is the splice acceptor site

5’ end - GT/GU in RNA for splicing on intron (Splice Donor Site)

NEcessary for splicing out introns from nascent RNA transcript before it leaves the nucleus

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42
Q

Pt undergoes an operation and then like 2 days later gets liver failure. Why?

A

HALOTHANE - idiosyncratic Hepatic Failure and Malignant Hyperthermia

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43
Q

What are signs/symptoms of congenital syphilis?

A

transmitted through the placenta to the fetus

Cleft palate, rhinitis, desquamating rash

Penicicilln Tx or if allergic use Doxycycline

MaBs to TNF may be beneficial

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44
Q

What are the cardioselective BEta blockers?

A

Indicated in low doses for use in pts w/ HTN and COPD

BEta 1 only: Metoprolol and ATenolol

increasing dose however lose beta1 selecitivty so be careful

(acebutolol, betaxolol, esmolol, atenolol, metoprolol)

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45
Q

what motor proteins are responsible for movement which way in the neuron/along the microtubules?

A

MT start w/ (-) end in the Centrosome (MTOC) and then radiate outwards w/ (+) ends

Kinesins go from neg to pos and so do anterograde transport
Dyneins go from pos to neg and so do retrograde transport

46
Q

What is Fomepizole?

A

Antidote for MEthanol and Ethylene glycol poisoining bc competitive antagonist of Alcohol Dehydrogenase thereby prevents conversion of the 2 substrates to toxic metabolites

47
Q

What is Filgrastim

A

Granulocyte Colony stimulating factor used w/ chemotherapy

48
Q

What’s so great about NAC? What is it used for?

A

1) ACetminophen OD enhances Glutathione production and conjugation to toxic NAPQI intermediate
2) Mucolytic agent in influenza, bronchitis, CF
3) Renal insufficiency w/ IV contrast NAC prevents radio-contrast induced nephrotoxicity

49
Q

What do you give w/ Cisplatin and why?

A

Armifostine - reduces free radical nephrotoxity (ATN) by scavenging free radical

+

Cl diuresis bc Cisplatin less active in high concentrations CL

50
Q

How do human cancer cells become resistant to chemotherapy?

A

ATP-dependent transporter changes

human multidrug resistance gene MDR1
P-glycoprotein that is ATP-dependent efflux pump and so ATP powered pump (normally in kidneys and intestine and at BBB border) actively removes chemotherapuetics (esp hydrophobic agents like Anthracyclines)

Drugs like Verapamil, Diltiazem and Ketoconazole reduce actions of MDR1 protein

SPECIFICITY for hydrophoic compounds

51
Q

What does CMV infection cause in immunocompetent ppl?

A

when CMV results in clinically relevant disease in immunocompetent, see systemic MONO-like syndrome w/ fever, malaise, myalgia, atypical lymphocytosis and elevated liver transaminases

but NO hterophil antibodies

52
Q

What are the NNRTIs and how do they work?

A

RT inhibitors that prevent synth of viral DNA from RNA and do not require activation via intracellular phosphorylation

Nevirapine, Efavirenz, Delavirdine

Adverse effects: Abrupt onset flu, abdominal pain, jauundice or fever - could be life threatening hepatic encephalopathy

or Stevens Johnson or Toxic Epidermal Necrolysis

53
Q

Pt has normocytic anemia that had low reticulocytes and low Hb - Pure Red Cell Aplasia. What could be the causes?

A

hypoplasia of marrow erythroid elements w/ normal granulopoeisis and thrombopoiesis involves inhibition of erythropoeitic precurosors and progenitors by IgG or cytotocxic T cells - AUTOIMMUNE

THYMOMA or LYMPHOCYTIC LEUKEMIA

or Parvovirus B19 - pro-erythroblasts

54
Q

What is normal PLatelet count?

A

150,000-400,000

55
Q

What is the most important cause of thrombocytopenia in hospitalized patients and how do you treat it?

A

Heparin!!!!

HIT more common w. use of UFH compared to LMWH and leads to paradoxical thrombosis rather than bleeding –> Abs to Heparin and PLatelet Factor 4

TX: Direct Thrombin INhibitors - Huridin, Lepirudin, Argotroban, Bivalrudin, Dabigatran do not require AT3 for action

Stop Heparin and give Direct Thrombin inhibitors

56
Q

Etoposide?

A

inhibits DNA Topoisomerase 2 from plant alkaloids

Topo 1 makes single strand nicks to relieve negative supercoiling and topo 2 induces transient breaks in both DNA strands to relieve positive and negative supercoiling

Etoposide inhibits Topo2’s ability to seal the dsDNA nicks causing chromosome breaks and cell death

TESTICULAR CANCER AND SMALL CELL LUNG CANCER

57
Q

What is Li Fraumeni Syndrome?

A

AD predisposition to cancers - Sarcomas and tumors of breast, brain and adrenal cortex

mutation in tumor suppressor gene P53

58
Q

Whats the mutation associated w. Mantle cell lymphoma?

A

Translocation of Cyclin D1 gene on Chromosome 11 to IG Heavy chain on CHromn 14

11;14 and increased Cyclin D1 to increase promoter of G1 to S phase

59
Q

What are the Antiplatelet drugs that block interaction of ligands w/ receptors?

A

Clopidogrel and Ticlopidine

ADP Antagonists

Treatment and prevention of ischemic strokes, acute coronary syndrome, and peripheral vascular disease

Additive effect w/ Aspirin

Ticlopidine only used when allergic to ASA and clopidogrel bc FX are bad: Neutropenia - fever and mouth ulcers

60
Q

What are the bad consequences of PNH?

A

PIGA gene mutation in hematoipoetic stem cells where no GPI anchor and so no C55 (DAF) or C59 (MAC) therefore complement hemolysis

Thrombotic complications (ex Budd Chiari) from free hb and platelet

Pancytopenia
Aplastic Anemia

TRIAD: Hemolytic Anemia, Hypercoagulability, and Pancytopenia

61
Q

What’s ERythema Infectiosium? What causes it?

A

Parvovirus B19!!! non-enveloped DNA virus

low grade fever, HA, malaise, URI followed by Slapped Cheeck rash 2-5 days later “Fifth Disease”

Then Reticular lacelike rash on extremities and trunk

Blood group P antigen, Globoside, expresson on RBC and receptor for virus –> Virus LOVES RBC PRECURSORS - Pronomoblasts and normoblasts and replicates in BM

62
Q

What factors are found in cryoprecipitate?

A

Factor 8, 13, VWF, and Fibrinogen

63
Q

What are side effects of steroid abuse?

A

Steroids usually ANDROGENS and Androgens increase RBC production and raise hematocrit!!! (also why men have higher HCt compared to women)

acne, voice deepening, male pattern bladness, livery effects

64
Q

What are lab values indicative of DIC?

A

elevated PT, PTT, abd bleeding time

D-Dimer increased - degradation product of crosslinked fibrin

65
Q

What are the HIV fusion inhibitors and CCR4 receptor inhibits?

A

Enfuvirtide - Fusion inhib - binds gp41 first heptad repeat and prevents it from undergoing change necessary to for viral membrane fusion

Maraviroc- CCR5 receptor inhibitor (gp120 must bind both C4 mlcl and chemokine receptor like CCR5 or CXCR4 and so this blocks attachment and entry)

66
Q

What are the RT inhibitors?

A

Efavirenz, Tenofovir, lamivudine

67
Q

What are the PRotease inhibitors for HIV>

A

“Navirs” like ritonavir

68
Q

What are the INtegrade inhibitors? for hiv duhh

A

GRAVIRS - Raltegravir

disrupts ability of ds HIV DNA to integrate into Host cells chromsomes and prevents host machinery from being used to synthesize HIV DNA

“Block mRNA transcription”

69
Q

What is Pentamidine used for?

A

PRophylaxis and treatment of Pneumocystis Jiroveci pneumonia in HIV patients

also can be used to treat Leishmanias and African Sleeping sickness

70
Q

What are the Malaria drugs?

A

ERythrocyte forms of parasites killed w/ either Chloroquine or Mefloquine

Primaquine required to kill P vivax and P ovale liver schizonts

71
Q

What are the most common tumors in kids?

A

Leukemia

Brain tumors

72
Q

Pilocytic Astrocytoma Presentation

A

1 most common brian tumor in kids (MEdulloblastoma #2, Ependymoma #3)

Kid w/ HA and Wide based stance

Cyst w/ Mural nodule

Cerebellum astrocyte tumor w/ Rosenthal Fibers
Good prognosis

73
Q

What’s most common malignant brain tumor of childhood?

A

Medulloblastoma

Cerebellum - Vermis
Sheets of small blue cells w/ hyperchromatic nuclei and scant cytoplasm
poor prognosis

74
Q

Ependymoma in kids presentation?

A

Ependymal cell lining of ventricle and can obstruct CSF flow

therefore present w/ Hydrocephalus
form gland-like structures called “Rosettes”

75
Q

What is Aplastic Anemia? how does it present and what happens?

A

Pancytopenia, low reticulocytes, no splenomegaly

Bone MArrow is hypocellular and replaced by fat cells and fibrous stroma - Dry Tap

***Pancytopenia and NO splenomegaly

76
Q

What is the most common primary brain neoplasm in adults? How does it present?

A

GBM - necrosis, pseudopallisading, new vessel formation, small round cells, bizarre giant cells, lots of mitoses

40-70 yo Astrocytoma in Frontal and temporal lobes and BAsal Ganglia and Crosses the Midline (butterfly)

Necrosis and Hemorrhage grossly

HA, Seizure, mental status change or neuro deficits

77
Q

What are presentations of different patterns of inheritence?

A

XLR - like G6PD deficiency mostly men
XLD - man affected will 100% have daughter affected - VitD resistant rickets

AD - structural problems like Hereditary Spherocytosis

AR - enzyme deficiency problems

78
Q

2 TX for Sickle Cell disease and mechanisms?

A

1) Hydroxyurea - increases HbF synthesis giving protection against polymerization
2) Preventing intracellular dehydration w/ Gardos channel blockers - Ca-dependent K channel regulates transport of K and Water through RBC membrane and so block and preventing dehydration erythrocytes

79
Q

What does anaplasia mean and what are some examples?

A

Anaplastic - Complete lack of differentiation and bear no resemblence to tissue of origin

Loss of cell polarity and disruption of architecture - sheets or islands disorganized

Nuclear pleomorphism
Large nuclei, coarse chromatin, hyperchromatic
mitotic figures

**GIANT MULTINUCLEATED TUMOR CELLS like in brain tumor

80
Q

What cancers do you get w/ RB mutation?

A

Retinoblastomas (duh) and Osteosarcomas and others (breast adenocarcinoma, small cell carcinoma of lung, bladder carcinoma)

Chromosome 13q14 encodes nuclear phosphotprotein RB that is either active (Hypophosphorylated) or inactive (hyperphosphorylateD)

Inactive allows cell to go from G1 –> S phase

81
Q

How can you get DIC in pregnancy? What happens? Labs?

A

Fetus dies and retained in utero then release Thromboplastic from placenta and activate Intravascular coagulation - widespread deposition of fibrin and consumption of coag factors, platelets, eventual bleeding and death

Decreased Fibrinogen and Factor 5 and 8 levels, decreased platelets, PT and PTT are prolonged , schistocytes

Plasmin activates fibrinolysys and releases D-Dimers into blood

**MONITOR FIBRINOGEN LEVELS AND PLATELET LEVELS

82
Q

N Myc vs C Myc

A

C-Myc - chromsome 8 (8;14 = Burkitts Lymphoma)
- oncogene and high grade lymphoma

N-Myc - oncogene in Neuroblastoma and Small CEll carcinoma of lung

83
Q

What happens in Myelofibrosis?

A

Chronic Myeoloproliferative disorder where clonal hematopoietic stem cell proliferation and ATYPICAL MEGAKARYOCYTE hyperplasia

Activates fibroblast proliferation and slow replacement of BM w/ Extensive collagen deposition

EArly Stage = BM Hypercellular
Later Stage = BM Fibrosis and Pancytopenia

SPLENOMEGALY - extramedullary hematopoiesis (unlike aplastic anemia)

84
Q

Myeloproliferative disease Mutation??

A

JAK2 gene - therefore hematopoeitic cells are more sensitive to Growth Factors like EPO and Thrombopoeitin

85
Q

Symptoms of PV?

A

Increased Hematocrit, RBC,

HA

86
Q

What are some receptor Tyrosine Kinases?

A

Insulin, IGF1, EGFR

Intrinsic Tyr Kinase activity and autophosphorylation

(Vs JAK2 which is a non-receptor Tyrosine Kinase)

87
Q

What is the medium used for Neisseria Gonorrhoea?

A

Thayer Martin or VCN - Selective Media

Vancomycin- Gram POs
Colistin - other gram negs
Nystatin - fungi

88
Q

What is Differential MEdia and give the most common example?

A

Differential media differentiate cultures based on metabolic and biochemical properties

example: Lactose fermenters appear purple/pink on Maconkey agar and Black on EMB Agar

89
Q

DEscribe the Microbiology characteristics of Pseudomonas

A

Motile, Aerobic, GN rod

Nonlactose Fermenting, Oxidase Positive

Produces Pyocyanin - blue green pigment

Grapelike odor

Endotoxin - fever and shock
Exotoxin A - inactivates EF 2

90
Q

Name the drugs used against Pseudomonas

A

Aminoglycosides
Piperacillin, Ticarcillin Penicillins

3rd and 4th generation cephalosporins (ceftazidime and cefepime)

Quinolones (ciprofloxacin)

Aztreonam (monobactam)

Carbapenems - Ima and Mero

91
Q

What is a Keiser Fleischer ring?

A

Brown ring around the iris

Wilsons Disease (or chroniic cholestatic disease like Primary billiary cirrhosis)

Best observed with slit lamp but can be seen grossly

COPPER DEPOSITION in Descemets membrane in Cornea

92
Q

Sup w/ Wilson’s Disase?

A

AR disease in ppl 4-50 yo
Mutations hinder Cu metabolism and so reduce formation and secretion of ceruloplasmin ANd decrease hepatic secretion of copper

Cu is Pro-Oxidant and damages hepatocytes and then leaks into circulation and deposits in Cornea and Basal Ganglia - ATROPHY OF BASAL GANGLIA

Copper Chelators like D-Penicillamine and Trientine

93
Q

What cell lineage are Ewing Sarcoma cells?

A

Neuroectodermal

94
Q

describe Efficacy vs Potency in Pharmodynamics

A

Efficacy = ability of drug to elicit effect - Emax ….Max ceiling effect

Potency = dose of drug required to produce given effect - Affinity of drug for receptor and amount of drug able to reach target tissue
- compare w/ dose of drug required to produce 50% maximal response (ED50) …lower ED50 then more potent

95
Q

What is Vd? What does high vs low Vd mean?

A

Vd = hypothetical volume of fluid into which the administered amt of drug would need to be uniformly distributed to produce observe plasma concentration

Vd (L) = Amount of drug given (mg) / Plasma concentration of drug (mg/L)

Low Vd (3-5 L) = Large Mlcl weight, bound to lots of plasma prtoein, or highly charged then remains in plasma compartment

small mlcl weight but hydrophillic it can distribute to ISF outside BV as well as intravascular and so Vd = 14-16 L (plasma + Interstitial)

Large Vd (41L) = small molecular and hydrophobic/uncharged then can reach intracellular compartment

Even HIGHER if bind avidly in tissues and accumulate there while maintaining low plasma concentrations

96
Q

Name two commonly used drugs that exhibit Tachyphylaxis

A

Alpha Adrenergic Topical agents (phenylephrine, Xylometazoline, Oxymetazoline) cause Rebound Rhinorrhea ….. Topicals > 3 days stop working bc decreased endogenous NE in nerve terminals and so relative vasodilation and congestion

Nitroglycerine - decrease effect bc diminished release of NO from target cells so need 8-10 hours of drug free intervals

97
Q

Rinne and Webber - GOTTA KNOW IT!!! Type of HEaring Loss? Side? CAuses?

A

Conductive HEaring Loss: Rinne test abnormal in affected ear (bone > air) and Webber TEst localizes to affected ear
- causes include cerebrum impaction, otosclerosis, tumors, tympanic membrane rupture, severe otitis

Sensorineural Hearing Loss: Rinne Test normal in both ears (air> bone) and Webber Test Localizes to UNAFFECTED ear
- causes include acoustic neuroma, presbyscusis, ototoxic drugs, Meniere Disease

98
Q

How is ISoniazid metabolized?

A

Acetylation to N-acetyl-isoniazid in hepatic microscomal system by N-acetyl transferase and then excreted in the urine

Slow vs Fast Acetylators: Dapsone, Hydralazine, PRocainamide so slow accumulate more fo these drugs and increased risk toxic effects vs fast much higher doses needed

99
Q

Describe the Cholesterol drugs effects on cholesterol synthesis.

A

STatins decrease cholesterol synthesis at the rate limiting step making malevonate

Cholesteryamine and bile acid binding agents increase hepatic cholesterol prodction independently

….when used together they net decrease hepatic cholesterol snth and plasma LDL levels

Fibrates and bile acid binding agents used together both increase cholesterol synthesis and associated w/ increased risk of gall stones

100
Q

What cytokines stimulate IGE production?

A

Th2 release IL13 and IL4 to promote IgE production

IL5 used to activate eosinophils

101
Q

What cytokines do what?

A

HOT T Bone stEAK

IL 1 fever
IL 2 T cells
IL 3 Bone marrow - GM - CSF
IL 4 IgE and IgG
IL 5 IgA and eosinophils
IL 6 AKute phase reactants

IL 8 = PMNs

102
Q

What’s the mechanism of ACtion of Terbinafene?

A

inhibits Squalene epoxidase to block sythesis of ergosterol for the fungal membrane

used for tinea dermatophytoses

103
Q

What are the side effects of protease inhibitors (navirs) used in HIV treatment?

A

REversibly bind viral protease and stop replication of HIV virus

Lipodystrophy - increased deposition of fat on the back and abdomen, deacreased adipose in extremities, Bufallo hump

Hyperglycemia - insulin resistance and may lead to frank diabetes

Inhibition of P450 - do NOT use rifampin w/ this bc will decrease levels of protease inhibitor, use w/ Rifabutin instead for mycobacterial infections

104
Q

What nerve and clinical manifestation occur w/ radical mastectomy?

A

damage to long thoracic nerve causes paralysis of serratus anterior muscle and winging of scapula

105
Q

What nerve can be damaged w/ crutches and what does this cause?

A

Radial nerve can get damaged with crutches (or mid humerus shaft break along with Brachial artery) and can lead to Wrist drop - failure to extend forearm and wrist

located superfillially in axilla

106
Q

What are the causes of cirrhosis? What Enzyme values do you see with the big ones?

A

Chronic EtOH, Hep B or C, Hemochromatosis, Wilson disease, A1At

EtOH AST and ALT elevated 2-7x the normal upper limit and AST:ALT > 1

Acute Viral Hepatitis has levels between 400-4000 with ALT> AST

107
Q

What are the signs/symptoms of Multiple Myeloma?

A

CRAB

hyperCalcemia - secretion of IL1 activates Osteoclasts (and IL6)
Renal involvement
Anemia - normocytic and normochromic anemia from BM replacement
Bone lytic lesions and Back pain

Monoclonal M spike

BM with greater than 30% plasma cells

108
Q

How does Carbon Tetrachloride cause injury?

A

Free radical injury

Oxidized in liver by P450 and greats free radical CCl3 which reacts w/ structural lipids of cell membranes and forms H2O2

LIPID PEROXIDATION

109
Q

Where are the P450 enzymes located?

A

MICROSOMES of Hepatocytes and ER of varied other tissues

110
Q

Name some common Proto-oncogenes and their cancers

A

RAS - bladder, lung, pancreas, kidney

N-Myc - neuroblastoma, Small cell carcinoma of lung

ERB-B1 - squamos cell carcinoma of lung

ERB-B2 - BReast and ovarian cancer

TGFalpha- astrocytoma, HCC

Sis - astrocytoma, Osteosarcoma

Abl - CML and ALL

111
Q

Name some tumor suppressor genes and their cancers

A

BRCA1/2 - DNA repair genes breast and ovarian

NF1 - Neuroblastoma, NF1, Sarcomas

APC/Beta-Catenin - Gastric, Colon, Pancreatic, Lynch syndrome

DCC - colon cancer

p53- Most cancers, Lifraumeni

Rb - Retinoblastoma, Osteosarcoma

WT-1 Wilms tumor

112
Q

What are the PAraneoplastic diseases seen by the different lung cancers?

A

Small cell Carcinoma - ACTH and Vassopressin or abs to Ca channel (Lambert Eaton) or abs to neurons (Paraneoplastic encephalitis/myelitis)

Squamous cell carcinoma - PTHrP and Hypercalcemia

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