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Focused Memorization > Things to just fucking memorize > Flashcards

Things to just fucking memorize Flashcards

1
Q

Functions of a1-receptors

A

Increase in vascular smooth muscle contraction
Increase in pupillary dilator muscle contraction
Increase intestinal and bladder sphincter muscle contraction

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2
Q

G-protein class of a1 receptors

A

q

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3
Q

Functions of a2 receptors

A 
Decrease in sympathetic outflow
Decrease insulin release
Decrease in lipolysis 
Increase platelet aggregation
Decrease aqueous humor
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4
Q

G-protein class of a2 receptor

A

i

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5
Q

Functions of B1 receptors

A

Increase heart rate
Increase contractility
Increase RENIN release
Increase lipolysis

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6
Q

G-protein class of B1

A

s

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7
Q

Functions of B2 receptors

A 
Vasodilation
Bronchodilation
Increase in lipolysis 
Increase insulin release 
Decrease in uterine tone
Increase aqueous humor production
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8
Q

G-protein class of B2

A

s

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9
Q

Functions of M1 receptors

A

CNS, enteric nervous system

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10
Q

G-protein class of M1

A

q

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11
Q

Functions of M2 receptors

A

Decrease heart rate and contractility of atria

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12
Q

G-protein class of M2

A

i

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13
Q

Function of M3 receptor

A

Increase exocrine glad secretions
Increase gut peristlsis
Increase bladder contraction
Ciliary muscle contraction

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14
Q

G-protein class of M3 receptor

A

q

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15
Q

Functions of D1 receptors

A

Relaxes renal vascular smooth muscle

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16
Q

G-protein class of D1

A

s

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17
Q

Functions of D2 receptors

A

Modulates transmitter release, especially the brain

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18
Q

G-protein class of D2

A

i

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19
Q

Functions of H1 receptors

A 
Increase nasal and bronchial mucus production
Increase vascular permeability
Contraction of bronchioles
Pruritus 
Pain
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20
Q

G-protein class of H1

A

q

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21
Q

Functions of H2 receptors

A

Increase gastric acid secretion

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22
Q

G-protein class of H2

A

s

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23
Q

Function of V1 receptors

A

Increase vascular smooth muscle contraction

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24
Q

G-protein class of V1

A

q

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25
Q

Function of V2 receptors

A

Increase water permeability and reabsorption in collecting tubules of kidney

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26
Q

G-protein class of V2

A

s

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27
Q

G-protein class associated with cAMP

A

Gs

Gi (inhibitory of Adenylyl cyclase)

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28
Q

G-protein class associated with increased [Ca2+] in heart

A

Gs

Gi (inhibitory of Adenylyl cyclase)

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29
Q

G-protein class associated with Increased [Ca2+] in smooth muscle contraction

A

Gq

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30
Q

Effect and applications of Albuterol, salmeterol

A

B2>B1

Albuterol for acute asthma; salmeterol for long-term asthma or COPD control

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31
Q

Effect and applications of Dobtamine

A

B1>B2, a

Heart failure,(inotropic > chronotropic)
Cardiac stress testing

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32
Q

Effect and applications of Dopamine

A

D1 = D2 > B > a

Unstable bradycardia, HF, shock,

Inotropic and chronotropic a effects predominate at high doses

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33
Q

Effect and applications of Epinephrine

A

B > a

Analphylaxis, asthma, open-angle glaucoma
a-effects predominate at high doses
Significantly stronger effect at B2-receptor than norepinephrine

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34
Q

Effect and applications of Isoproterenol

A

B1 = B2

Electrophysiologic evaluation of tachyarrythmias. Can worsen ischemia.

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35
Q

Effect and applications of Norepinephrine

A

a1 > a2 > B1

Hypotension (but decrease renal perfusion)
Significantly weaker effect at B2-receptor than epinephrine

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36
Q

Effect and applications of Phenylephrine

A

a1 > a2

Hypotension (vasoconstrictor)
Ocular procedures
Rhinitis

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37
Q

Effect and applications of Amphetamine

A

Indirect general agonist, reuptake, inhibitor, also releases stored catecholamines

Used in narcolepsy, obesity, ADHD

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38
Q

Effect and applications of Cocaine

A

Indirect general agonist, reuptake inhibitor

Causes vasoconstriction and local anesthesia.

Never give Beta-blockers if cocaine intoxication is suspected (can lead to unopposed a1 activation and extreme hypertension)

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39
Q

Effect and applications of Ephedrine

A

Indirect general agonist, releases stored catecholamines

Used in: Nasal decongestion, urinary incontinence, hypotension

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40
Q

IL-1

A

Secreted by Macrophages

Also called osteoclast-activated factor.
Causes fever, acute inflammation. Activates endothelium to express adhesion molecules. Induces chemokine secretion to recruit WBCs.

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41
Q

IL-2

A

Stimulated by All T-Cells

Stimulates growth of helper, cytotoxic and regulatory T cells, and NK cells

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42
Q

IL-3

A

Secreted by All T-Cells

Supports growth and differentiation of bone marrow stem cells. Functions like GM-CSF

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43
Q

IL-4

A

Secreted from Th2 Cells

Induces differentiation into Th2 cells. Promotes growth of B cells. Enhances class switching to IgE and IgG

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44
Q

IL-5

A

Secreted from Th2 Cells

Promotes differentiation of B cells. Enhances class switching to IgA. Stimulates growth and differentiation of eosinophils

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45
Q

IL-6

A

Secreted by Macrophages

Causes fever and stimulates production of acute-phase proteins

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46
Q

IL-8

A

Secreted by Macrophages

Major chemotactic factor for neutrophils

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47
Q

IL-10

A

Secreted from Th2 cells

Modulates inflammatory response. Decreases expression of MHC class II and Th1 cytokines. Inhibits activated macrophages and dendritic cells. Also secreted by regulatory T cells

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48
Q

IL-12

A

Secreted by Macrophages

Induces differentiation of T cells into Th1 cells. Activates NK cells

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49
Q

Interferon-gamma

A

Secreted from Th1 cells

Secreted by NK cells in response to IL-12 from macrophages; stimulates macrophages to kill phagocytosed pathogens.

Also activates NK cells to kill virus-infected cells. Increases MHC expression and presentation by all cells.

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50
Q

TNF-a

A

Secreted by macrophages

Mediates septic shock. Activates endothelium. Causes WBC recruitment, vascular leak.

Causes cachexia in malignancy

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51
Q

What cytokines are secreted by Macrophages?

A 
IL-1
IL-6
IL-8
IL-12
TNF-a
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52
Q

What cytokines are secreted by All T-Cells?

A

IL-2

IL-3

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53
Q

What cytokines are secreted from Th1 cells?

A

Interferon-gamma

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54
Q

What cytokines are secreted from Th2 cells?

A

IL-4
IL-5
IL-10

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55
Q

Whats a helpful pneumonic for remembering the actions of IL-1 through IL-6?

A

Hot T-Bone stEAK

IL-1: Fever
IL-2: stimulated T-cells
IL-3: stimulates Bone marrow
IL-4: stimulates IgE production 
IL-5: stimulates IgA production 
IL-6: stimulates aKute-phase protein production
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56
Q

What are the Helper T cells?

A

Th1 and Th2

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57
Q

What do Th1 cells do?

A

Activate macropahges and cytotoxic T cells

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58
Q

What activates Th1 cells?

A

INF-y and IL-12

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59
Q

What inhibits Th1 cells?

A

IL-4 and IL-10 (from Th2 cells)

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60
Q

What do Th2 cells do?

A

Recruits eosinophils for parasite defense and promotes IgE production by B cells

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61
Q

What activates Th2 cells?

A

Activated by IL-4

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62
Q

What inhibits Th2 cells

A

IFN-y (from Th1 cells)

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63
Q

HLA subtypes associated with disease:

A3

A

Hemochromatosis

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64
Q

HLA subtypes associated with disease:

B27

A

“PAIR”

Psoriatic arthritis, Anklosing spondylitis, arthritis of of Inflammatory bowel disease, Reactive arthritis

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65
Q

HLA subtypes associated with disease:

DQ2/DQ8

A

Celiac disease

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66
Q

HLA subtypes associated with disease:

DR2

A

MS
hay fever
SLE
Goodpasture

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67
Q

HLA subtypes associated with disease:

DR3

A

Diabetes mellitus type 1, SLE, Graves disese, Hashimoto thyroiditis

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68
Q

HLA subtypes associated with disease:

DR4

A

Rheumatoid arthritis, DM1

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69
Q

HLA subtypes associated with disease:

DR5

A

Pernicious anemia&raquo_space; Vit B12 deficiency

Hashimoto thyroiditis

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70
Q

Bacterial infections associated with decreased T-cells

A

Sepsis

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71
Q

Bacterial infection associated with decreased B cells

A 
Encapsulated:
Step. pneumo
H. flu
N. meningitidis
E. coli 
Salmonella
Klebsiella pneumoniae
Group B strep
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72
Q

Bacterial infections associated with decreased granulocytes

A 
Staph
Burkholderia cepacia
Pseudomonas
Serratia
Nocardia
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73
Q

Bacterial infections associated with decreased complement

A

Encapsulated species with early component deficiences

Neisseria with late component (MAC) deficiences

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74
Q

Viral infections associated with decreased T cells

A 
CMV
EBV
JCV
VZV
Chronic infection with respiratory/GI viruses
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75
Q

Viral infections associated with decreased B cells

A

Enteroviral encephalitis

Poliovirus

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76
Q

Fungal/parasitic infections assoicated with decreased T cells

A

Candida (local)

PCP

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77
Q

Fungal/parasitic infection associated with decreased B cells

A

GI giardiasis (no IgA)

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78
Q

Fungal/parasitic infection associated with decreased granulocytes

A

Candida (systemic)

Aspergillus

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79
Q

What structures transverse the Cribiform plate?

A

CN I olfactory bulbs

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80
Q

What structures transverse the Optic canal?

A

CN II, opthalmic artery, central retinal vein

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81
Q

What structures transverse the Superior orbital fissure?

A

CNII, IV, V(1), VI, opthalmic vein, sympathetic fibers

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82
Q

What structures transverse the Foramen Rotundum?

A

CN V(2) (Maxillary)

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83
Q

What structures transverse the Foramen Ovale?

A

CN V(3) (Mandibular)

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84
Q

What structures transverse the Foramen Spinosum

A

Middle meningeal artery and vein

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85
Q

What structures transverse the Internal Acoustic Meatus

A

CN VII, VIII

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86
Q

What structures traverse the Jugular foramen?

A

CN IX, X, XI, jugular vein

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87
Q

What structures traverse the Hypoglassal canal?

A

CN XII

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88
Q

What structures traverse the Foramen Magnum?

A

Spinal roots of CN XI, brain stem, vertebral arteries

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89
Q

Enzyme deficiency in Sideroblastic anemia

A

∂-aminolevulinic acid synthase
Glycine + succinyl CoA&raquo_space;> ∂-aminolevulinic acid

NEEDS Vit B6!

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90
Q

Enzyme deficiency in Lead poisoning

A

∂- aminolevulinic acid dehydrogenase:
∂-aminolevuliic acid&raquo_space;> Porphobilinogen

Ferrochelatase:
Protoporphyrin&raquo_space;> Heme

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91
Q

Enzyme deficiency in Acute intermittent porphyria

A

Porphobilinogen deaminase

Porphobilinogen&raquo_space;> Hydroxymethylbilane

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92
Q

Enzyme deficiency in Porphyria cutanea tarda

A

Uroporphyrinogen decarboxylase

Uroporphyrinogen III&raquo_space;> Coproporphyrinogen III

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93
Q

Bernard Soulier syndrome

A

Defect in platelet plug formation

Decrease in GpIb (platelet-to-vWF adhesion)

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94
Q

Glanzmann thrombocytopenia

A

Defect in platelet plug formation

Decrease in GpIIb/IIIa (platelet aggregation)

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95
Q

Immune thrombocytopenia

A

Anti-GpIIb/IIIa antibodies&raquo_space; splenic macrophage consumption of platelet-antibody complex

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96
Q

Thrombotic thrombocytopenic purpura

A

Inhibition or deficiency of ADAMTS13&raquo_space;> decrease degradation of vWF multimers

Schistocytes seen

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97
Q

von Willebrand disease

A

Intrinsic pathway coagulation defect
Increase PTT
Tx with desmopressin, which releases vWF stored in endothelium

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98
Q

Vitamin K acts as cofactor for…

A

factors:
II, VII, IX, X
Protein C, S

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99
Q

Protein C&raquo_space; Protein S&raquo_space; cleaves…

A

Va, VIIIa

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100
Q

Plasminogin&raquo_space; (tPA)&raquo_space; Plasmin»> does what?

A

Fibrinolysis:
Cleavage of fibrin mesh
Destruction of coagulation factors

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101
Q

Translocation with Burkitt lymphoma

A

8:14

c-myc activation

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102
Q

Translocation with CML

A

9:22 (Philadelphia)

BCR-ABL, which overexpresses tyrosine kinase&raquo_space; cell division

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103
Q

Translocation with Mantle Cell lymphoma

A

11:14

Cyclin D1 activation

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104
Q

Translocation with Follicular lymphoma

A

14:18

BCL-2

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105
Q

Translocation in APL

A

15:17

responds to all-trans retinoic acid

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106
Q

Mutation associated with Chronic myeloproliferative disorders

A

JAK2

A non-receptor kinase protein. Leads to persistant activation of signal transducers and activators of transcription (STAT) proteins

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107
Q

MOA for MTX, 5-FU

A

Decrease thymidine synthesis

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108
Q

MOA for 6-MP

A

Decrease de novo purine synthesis

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109
Q

MOA for Hydroxyurea

A

Inhibits ribonucleotide reductase

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110
Q

MOA for Cisplatin/Alkylating agents

A

Cross linking DNA

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111
Q

MOA for Belomycin

A

DNA strand breakage

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112
Q

MOA for Dactinomycin, doxorubicin

A

DNA intercalators

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113
Q

MOA for Etoposide

A

Inhibits topoisomerase II

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114
Q

MOA for Irinotecan

A

Inhibits topoisomerase I

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115
Q

MOA for Vinca alkaloids

A

Inhibit microtubule formation

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4
5
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116
Q

MOA for Paclitaxel

A

Inhibits microtubule disassembly

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117
Q

CYP450 Inhibitors

A 
Acetaminophen, NSAIDs
Antibiotics/Antifungals
Trimethoprin-sulfamethoxazole
Amiodarone
Cimetidine 
Cranberry juice, Ginkgo biloba, Vit E
Omeprazole
Thyroid hormone
SSRIs (fluoxetine)
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118
Q

CYP450 Inducers

A 
Carbamazepine
Ginseng
Green veggies
Oral contraceptives
Phenobarbital
Phenytoin 
Rifampin
St Johns Wart
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119
Q

RAS oncogene

A

1-hit GAIN of function
GTP-binding protein

Cholangiocarcinoma
Pancreatic adenocarcinoma

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120
Q

MYC oncogene

A

1-hit GAIN of function
Transcription factor

Burkitt lymphoma

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121
Q

BRCA 1/2 oncogene

A

2-hit LOSS of function
DNA repair genes

Breast and ovarian cancer

122
Q

APC/ß catenin oncogene

A

2-hit LOSS of function
Wnt signaling pathway

Colon, gastric and pancreatic cancer
Familial adenomatous polyposis

123
Q

ERBB1 (EGFR) oncogene

A

1-hit GAIN of function
Receptor tyrosine kinase

Lung adenocarcinoma

124
Q

TP53 oncogene

A

2-hit LOSS of function
Genomic stability

Most cancers
Li-Fraumeni syndrome

125
Q

ERBB2 (HER2) oncogene

A

1-hit GAIN of function
Receptor tyrosine kinase

Breast cancer

126
Q

RB oncogene

A

2-hit LOSS of function
G1/S transition inhibitor

Retinoblastoma
Osteosarcoma

127
Q

ABL oncogene

A

1-hit GAIN of function
Nonreceptor tyrosine kinase

CML

128
Q

BRAF oncogene

A

1-hit GAIN of function
Ras signal transduction

Hairy cell leukemia
Melanoma

129
Q

VHL oncogene

A

2-hit LOSS of function
Ubiquinitin ligase component

Renal cell carcinoma
Von Hippel-Lindau syndrome

130
Q

WT1 oncogene

A

2-hit LOSS of function
Urogenital differentiation

Wilms tumor

131
Q

What does Gastrin do, and where does it come from?

A

Secreted from G cells in gastric antrum, duodenum

Increases gastric acid secretion

132
Q

What does Somatostatin do and where does it come from?

A

Secreted from D cells from the pancreatic islets and in gut mucosa

Decreases secretion of most GI hormones

133
Q

What does Cholecystokinin do and where does it come from?

A

Secreted from I cells in small intestine

Increases pancreatic enzyme and HCO3- secretion

134
Q

What is Secretin and where does it come from?

A

Secreted from S cells in the small intestine

Increases pancreatic HCO3- secretion
Decreases Gastric acid secretion

135
Q

What is GIP and where does it come from?

A

K cells in small intesting

Increases insulin release
Decreases Gastric acid secretion

136
Q

What is motilin and what does it do?

A

M cells in small intestine

Increases GI motility

137
Q

Drugs that can cause Steven Johnson Syndrome

A

Anti-epileptic drugs (especially lamotrigine)

Allopurinol

Sulfa drugs

Penicillin

138
Q

Drugs that can cause Drug-Induced Lupus

A

SHIPP-E

Sulfa drugs, Hydralazine, Isoniazid, Procainamide, Phenytoin, Etanercept

139
Q

P450 Inducers

A 
Chronic alcohol use
St Johns Wart
Phenytoin
Phenobarbital 
Nevirapine
Rifampin
Griseofulvin 
Carbamazepine

“Chronic alcoholics STeal PHEN-PHEN and NEver Refuse GReasy CARBs”

140
Q

P450 Inhibitors

A 
Acute Alcohol Abuse 
Ritonaer
Amiodarone
Cimetidine
Ketoconazole 
Sulfonamides
Isoniazid (INH)
Grapefruit juice 
Quinidine
Macrolides (except azithromcin)

“AAA RACKS IN GQ Magazine”

141
Q

P450 Substrates

A

Anti-epileptics
Theophylline
Warfarin
OCPs

“Always Think When Outdoors”

142
Q

List of Sulfa Drugs

A 
Probenecid
Furosemide
Acetazolamde
Celecoxib
Thiazides
Sulfonamide antibiotics 
Sulfasalazine
Sulfonyureas

“Popular FACTSSS”

143
Q

Live attenuated virus vaccines:

A

Induce humoral and cell-mediated immunity. Rarely revert back to virulence. No booster needed. Dangerous for immunocompromised patients.

Smallpox
Yellow fever
Rotavirus
Chickenpox
Sabin polio
MMR
Influenza (intranasal)
144
Q

Killed viral vaccines:

A

Induce ONLY humoral immunity. Stable, cannot revert.

Rabis
Influenza (injected)
Salk Polio
HAV

145
Q

Subunit viral vaccines:

A

HBV (antigen = HBsAg)

HPV

146
Q

Encapsulated bacteria vaccine

A

Contain polysaccharide capsule antigens that are conjugated to a carrier protein. (Polysaccharide antigen alone cannot be presented to T-cells). T-cell activation and subsequent class-switching.

Pneumococcal (two types: one is conjugated, one isn’t)
H. flu type B
Meningococcal

147
Q

Urease-positive organisms

A 
Cryptococcus 
H. pylori
Proteus
Ureaplasma
Nocardia
Klebsiella 
S. epidermidis
S. saprophyticus
148
Q

Obligate intracellular bugs

A

Rickettsia
Chlamydia
Coxiella

Rely on host ATP

149
Q

Facultative intracellular bugs

A 
Salmonella
Neisseria 
Brucella 
Mycobacteria 
Listeria 
Francisella
Legionella 
Yersinia pestis
150
Q

Encapsulated bacteria

A 
Streptococcus pneumoniae
H. flu type B
Neisseria
E. coli
Salmonella
Klebsiella
Group B strep

Are opsonized and then cleared by spleen. Increased infection for aslpenics

151
Q

Catalase-positive organisms

A 
Nocardia 
Pseudomonas
Listeria 
Aspergillus
Candida
E. coli 
Staph
Serratia
152
Q

Protein A virulence factor:

What bug uses it, and how does it work?

A

Expressed by S. aureus

Binds Fc region of IgG. Prevents opsonization and phagocytosis

153
Q

IgA protease virulence factor:

What bugs use it, and how does it work?

A

Secreted by S. penumoniae, H. flu type B and Neisseria

Cleaves IgA in order to colonize respiratory mucosa

154
Q

M protein virulence factor:

What bugs use it, and how does it work?

A

Expressed by group A Strep

Helps prevent phagocytosis. Shares similar epitopes to human cellular protein (molecular mimicry)- underlies the autoimmune response of rheumatic fever

155
Q

Exotoxin of Corynebacterium diphteriae

A

Diphtheria toxin

Inactivates EF-2

Pharyngitis with psudeomembranes in throat and severe lymphadopathy (bull neck)

156
Q

Exotoxin of Pseudomonas aeruginosa

A

Exotoxin A

Inactivates EF-2

Causes host cell death

157
Q

Exotoxin of Shigella spp.

A

Shiga toxin

Inactivates 60S ribosome by removing adenosine from rRNA

Causes GI mucosal damage, causing dysentery. Also enhances cytokine release, causing hemolytic-uremic syndrome

158
Q

Exotoxin of E. Coli (EHEC)

A

Shiga-like toxin

Inactivate 60S ribosome by removing adenine from rRNA

Enhances cytokine release, causing HUS.

159
Q

Exotoxin of Bacillus anthracis

A

Edema toxin

Mimics the adenylate cyclase enzyme (increase cAMP)

Likely responsible for characteristic edematous boarders of black eschar in cutaneous anthrax

160
Q

Exotoxin of Vibrio cholerae

A

Cholera toxin

Overactivates adenylate cylcase (increase cAMP) by permanently activating Gs, leading to and increase in Cl- secretion in gut and H2O efflux

Voluminous rice-water diarrhea

161
Q

Exotoxin in Bordetella pertussis

A

Pertussis toxin

Overactivates adenylate cyclase (increase cAMP) by disabling Gi, impairing phagocytosis to permit survival of microbe

Whooping cough

162
Q

Exotoxin of Clostridium tetani

A

Tetanospamin

Proteases that cleave SNARE. Prevents release of GABA and glycine from Renshaw cells in spinal cord

Spasticity, clonus, lockjaw

163
Q

Exotoxin of Clostridium botulinum

A

Botulinum toxin

Protease that cleave SNARE. Prevents release of ACh at NM junctions

Flaccid paralysis

164
Q

Exotoxin of Clostridium perfringens

A

Alpha toxin

Phospoliase that degrades tissue and cell membranes

Degradation of phopholipids leading to “gas gangrene” and hemolysis (double zone of hemolysis on blood agar)

165
Q

Exotoxin of Streptococcus pyogens - Cell membrane variety

A

Stretptolysin O

Protein that degrades cell membrane

Lyses RBCs; contributes to B-hemolysis. Host antibodies against toxin (ASO) are sued to diagnose rheumatic fever

166
Q

Exotoxin in Staph. aureus

A

Toxic Shock Syndrome Toxin (TSST-1)

Binds to MCH II and TCR outside of antigen binding site to cause overwhelming release of IL-1, IL-2, IFN-y, and TNF-a, leading to shock

TSS = fever, rash, shock.
Other toxins can cause scalded skin syndrome (exfoliative toxin) and food poisoning (enterotoxin)

167
Q

Exotoxin in Strep. pyogenes - shock variety

A

Exotoxin A

Binds to MCH II and TCR outside of antigen binding site to cause overwhelming release of IL-1, IL-2, IFN-y, and TNF-a, leading to shock

TSS= fever, rash, shock

168
Q

Affects fo Endotoxin

A

Use “ENDOTOXIN” to remember the main points)

Edema 
Nitric oxide release (hypotension)
DIC/Death
Outer membrane of most gram-negative is where its found
TNF-a
O-antigen
eXtremely heat stable 
IL-1
Neutrophil chemotaxis
169
Q

NPH insulin

A

Long acting, twice daily dosing

18 hours

170
Q

Glargine insuline

A

Long acting, once daily

24 hour duration

171
Q

Determir insulin

A

Long acting, once daily

24 hour duration

172
Q

Regular insulin

A

Short acting
Peaks 2-4 hours
Best for IV use in diabetic ketoacidosis

173
Q

Lispro insulin

A

Post-prandial

Peak 45-75 min

174
Q

Aspart insulin

A

Post-prandial

Peak 45-75 min

175
Q

Glulisine insulin

A

Post-prandial

Peak 45-75 min

176
Q

Cyclosporine: Cell Target and side effects

A

Inhibits calcineurin

Blocks T-cell activation by preventing IL-2 transcription

SI: Nephrotoxicity, hypertension, hyperlipidemia, gingival hyperplasia

177
Q

Tacrolimus (FK506): Cell Target and side effects

A

Inhibits Calcineurin; binds FK506 binding protein

Blocks T-cell activation by preventing IL-2 transcription

SI: Nephrotoxicity. Increased risk of diabetes and neurotoxicity. NO gingival hyperplasia

178
Q

Siroliumus (Rapamycin): Cell target and side effects

A

mTOR inhibitor. Binds FKPB. In cytoplasm.

Blocks T-cell activation and B-cell differentiation by preventing response to IL-2

SI: Anemia, thromobycopenia, leukopenia. NOT nephrotoxic (so its good for kidney transplants)

179
Q

Daclizumab, Basiliximab: Cell target and SI

A

Monoclonal antibodies, blocks IL-2R

MEMBRANE RECEPTOR inhibitor

SI: Edema, hypertension, tremor

180
Q

Azathioprine: Cell target and SI

A

Antimetabolite precursor of 6-mercaptopurine.

Inhibits lymphocyte proliferation by blocking nucleotide synthesis. Blocks PRPP amidotransferase (cytoplasm) so Purine nucleotides cannot take part in DNA replication (nucleus)

SI: Leukopenia, anemia, thrombocytopenia

6-MP degraded by xanthine oxidase, so toxicity is increased by allopurinol

181
Q

Glucocorticoids: Cell target and SI

A

Inhibit NF-kB. Suppress both B and T cell function by decreasing transcription of many cytokines. IN the NUCLEUS

182
Q

Atrial natriueretic peptdie

A

Released from atrial myocytes in response to increased blood volume and atrial pressure. Acts via cGMP
Causes vasodilation and lowers Na+ reabsorption at the renal collecting tubule
Dilates afferent renal arterioles and constricts efferent arterioles, promoting diuresis

183
Q

B-type (brain) natriuretic peptide

A

Released from Ventricular myocytes in response to increased tension. Similar physiologic action to ANP, with longer half life. BNP blood test in sued for diagnosing F

184
Q

Leads with ST elevation for LAD infarct

A

V1-V2

V3-V4 (distal LAD)

V5-V6 (LAD or LCX)

185
Q

Leads with ST elevation for LCX infarct

A

V5-V6 (LAD or LCX)

I, aVL

186
Q

Leads with ST elevation for inFerior RCA infarct

A

II, III, aVF

187
Q

The “6” nephrotic syndromes to remember

A

Minimal Change Disease
Focal Segmental Glomerulosclerosis

Membrane Nephropathy
Membranoproliferative (can also be nephritic)

Diabetes Mellitus
System Amyloidosis

188
Q

Examples of Nephritic Syndrome

A 
Alport Syndrome 
IgA Nephropathy 
Post-Streptococcal Glomerulonephritis 
Goodpastures
Diffuse Proliferative GN
Wegners
Churg-Staus
Microscopic polyangitis
189
Q

Minimal Change Disease

A

Nephrotic Syndrome

Associated with Hogkins Lymphoma
Idiopathic

Podocytes lose foot processes due to cytokine damage
Normal HE stain
ONLY albumin is lost. NOT immunoglobulins

Responds well to steroids

190
Q

Focal Segmental Glomerulosclerosis

A

Idiopathic
Seen in HIV, heroin use, Sickle Cell (so you know, brown people…ugh)

“Progression of MCD if it doesn’t respond to steroids”

191
Q

Membrane Nephropathy

A

Idiopathic
Seen in Lupus! Also Hep B, C, solid tumors, NSAID use

Thick basement membrane
“Spike and dome” appearance”

Immune complex deposition under foot processes. Granular, sub-epithelial

Antibodies to the PLA2-receptor found on podocytes

192
Q

Membranoproliferative GN

A

Can be Nephritic OR Nephrotic

Immune complex deposition

Type I: Subendothelial, more often “Tram Track” appearance”. Seen in Hep B, Hep C

Type II: Deposition WITHIN the basement membrane. Autoantibody of C3 nephritic factor. Stabilizes C3 convertase, increasing inflammation. (Low C3, High inflammation)

193
Q

Diabetic Mellitus Nephropathy

A 
Non-enzymatic glycosylation 
Hyline arteriolosclerosis (efferent vessel)
Thick vessel wall 
Give ACE-inhibitor! 
Kemmelstiel-Wilson nodules!!
194
Q

Systemic Amyloidosis Nephropathy

A

Congo-red stain
Apple green bifringence
Kidney is most commonly affected organ in amyloidosis

195
Q

Alport Syndrome

A

X-linked disorder of IV collagen

Thinning and splitting GBM
Isolated hematuria
Sensory hearing loss, eye problems

196
Q

Post-Streptococcal GN

A

M-protein virulence factor
Immune complex (granular)
Sub-epithelial hump
Supportive tx

Adults can develop Rapidly Progressive GN, creating crescents in Bowman’s Space (composed for macrophages and fibren)

197
Q

IgA Nephropathy

A

Deposits in mesangium

Can progress to renal failure

198
Q

Goodpastures

A

Antibodies to the Basement membrane (alpha3-chain of collagen type IV)
Linear IgG and C3 deposition

199
Q

Diffuse proliferative GN

A

Lupus!

Granular IF deposits

200
Q

Wegeners

A 
c-ANCA
Affects Nose, Lung, Kidney 
Pauci-immune
Sinus problems!!
NO linear complex (not immune complexes, instead, c-ANCA)
201
Q

Churg-Staus

A 
p-ANCA
Granulomatous 
EOSINOPHILIA 
ASTHMA 
Can involved GI tract, CV system. Commonly vasculitis affecting the epineural vessels (can see a wrist drop, for example)

Frequent laboratory finding: antibodies against neutrophil myeloperoxidase

202
Q

Microscopic Polyangitis

A

p-ANCA

NO eosinophilia or asthma

203
Q

Anti-oncogenes (therefore inactivated in cancer)

A

APC
BRCA1
RB
TP53

204
Q

Burkitt Lymphoma; associations

A

Adolescents or young adults

“Starry sky” appearance
Associated with EBC
Jaw lesion = Africa
Pelvis/Abdomen = Sporadic

205
Q

Burkitt Lymphoma; genetics

A

t(8;140

c-myc

206
Q

Diffuse Large B-cell lymphoma; associations

A

Older adults, 20% in kids

Most common type of non-Hodgkin lymphoma in adults

207
Q

Follicular lymphoma; associations

A

Adults

Presents with “waxing and waning” lymphadenopathy. Nodular, small cells; cleaved nuclei

Bcl-2 inhibits apoptosis

208
Q

Follicular lymphoma; genetics

A

t(14;18) translocation of heavy-chain Ig (14) and BCL-2 (18)

209
Q

Mantle cell lymphoma; associations

A

Older males

CD5+

210
Q

Mantle cell lymphoma; genetics

A

t(11;14)

Translocation of cyclin D (11) and heavy-chain Ig (14)

211
Q

Adult T-cell lymphoma

A

Adults

Caused by HTLV (associated with IV drug abuse)

Present with cutaneous lesions; especially affects population in Japan, West Africa and Caribbean.

Lytic bone lesions, hypercalcemia

212
Q

Mycosis fungiodes/Sezary

A

Adults

Presents with skin patches/plaques (cutaneous T-cell lymphoma)

Atypical CD4+ cells with “cerebriform” nuclei. May progress to Sezary syndrome (T-cell luekemia)

213
Q

Multiple Myeloma; symptoms

A 
CRAB:
HyperCalcemia 
Renal involvement 
Anemia 
Bone lytic lesions/Back pain 
Monoclonal M protein  spike

Associated with increased susceptibility to infection and Primary amyloidosis

214
Q

Multiple Myeloma; histologic/diagnostic findings

A

Ig light chain in urine
Rouleaux formation
Numerous plasma cells with “clock face” chromatin and intracytoplasmic inclusions containing immunoglobulin
Monoclonal plasma cells = “fried egg” appearance

215
Q

Myelodysplastic syndromes

A

Stem cell disorders involving ineffective hematopoiesis

Caused by de novo mutation or environmental exposure (radiation, benzene, chemotherapy)

Risk of transformation to AML

216
Q

Acute lymphoblastic leukemia/lymphoma (ALL); associations

A 
Under 15 years old
Down syndrome 
Peripheral blood and bone marrow have increased lymphoblasts 
TdT+ marker (pre-T and pre-B)
CD10+ (pre-B)

May spread to CNS and testes

217
Q

Acute lymphoblastic leukemia/lymphoma (ALL); genetics

A

t(12;21)

218
Q

Chronic lymphoblastic leukemia

/small lymphocytic lymphoma

A

Older than 60 years
Most common adult leukemia

Often asymptomatic, progresses slowly

Smudge cells seen in peripheral smear

Autoimmune hemolytic anemia

CD20+, CD5+ B-cell neoplasm

219
Q

Hairy Cell Leukemia

A

Adults

Mature B-cell tumor

Dry tap bone marrow

Stains TRAP

Tx: cladribine, pentostatin

220
Q

Acute myelogenous leukemia (AML); associations

A

Median age ~65

Auer rods
Cytoplasmic inclusions
Increase in circulating myeloblasts

Down Syndrome

Risk: exposure to alkylating chemotherapy, radiation, myeloproliferative disorders

M3 AML responds to all-trans retinoic acid

DIC is a common presentation

221
Q

Acute Myelogenous Leukemia; genetics

A

t(15;17)

222
Q

Chronic Myelogenous Leukemia (CML)

A

Peak incidence 45-85 years

Myeloid stem cell proliferation;

Presents with increased neutrophils, metamyelocytes, basophils, splenomegaly

May transform to AML or ALL (blast crisis)

Responds to imatinib

223
Q

Chronic Myelogenous Leukemia (CML); genetics

A

Philadelphia chromosome

t(9;22)

224
Q

Region of the BRAIN most at risk for ischemic damage

A

ACA/MCA/PCA boundary areas

225
Q

Region of the HEART most at risk for ischemic damage

A

Subendocardium (LV)

226
Q

Region of the KIDNEY most at risk for ischemic damage

A

Straight segment of proximal tubule (medulla)

Thick ascending limb (medulla)

227
Q

Region of the LIVER most at risk for ischemic damage

A

Area around central vein (zone III)

228
Q

Region of the COLON most at risk for ischemic damage

A

Splenic flexure

Rectum

229
Q

Paraneoplastic Syndrome: Acanthosis nigricans

A

Gastric adenocarcinomas and other visceral malignancies

230
Q

Paraneoplastic Syndrome: Sign of Leser-Trelat (an explosion of seborrheic keratoses)

A

GI adenocarcinomas and other visceral malignancies

231
Q

Paraneoplastic Syndrome: Hypercalcemia

A

PTHrP

Squamous cell carcinomas of lung, head, neck

Renal, bladder, breast, ovarian carcinomas

In lymphoma, is by the mechanism of increased 1,25(OH2) Vitamin D3

232
Q

Paraneoplastic Syndrome: Cushing Syndrome

A

Increase in ACTH

Small cell lung cancer

233
Q

Paraneoplastic Syndrome: Hyponatremia (SIADH)

A

Increase in ADH

Small cell lung cancer

234
Q

Paraneoplastic Syndrome: Polycythemia

A

Increase in Erythropoietin

Renal cell carcinom
Hepatocellular carcinoma
Hemangioblastoma 
Pheochromocytoma 
Leiomyoma
235
Q

Paraneoplastic Syndrome: Pure re cell aplasia

A

Anemia with low reticulocytes

Thymoma

236
Q

Paraneoplastic Syndrome: Trousseau Syndrome

A

Migratory superficial thrombophlebitis

Adenocarcinomas, especially pancreatic

237
Q

Paraneoplastic Syndrome: Nonbacterial thromboic endocarditis

A

Deposition of sterile platelet thrombi on heart valves

Adenocarcinomas, especially pancreatic

238
Q

Paraneoplastic Syndrome: Anti-NMDA receptor encephalitis

A

Psychiatric disturbance, memory deficits, seizures, dyskinesias, autonomic instability, language dysfunction

Ovarian teratoma

239
Q

Paraneoplastic Syndrome: Opsoclonus-myoclonus ataxia (“Dancing eyes, dancing feet”)

A

Neuroblastoma (children)

Small cell lung cancer (adults”

240
Q

Paraneoplastic Syndrome: Antibodies against Hu, Yo and Tr antigens in Purkinje cells

A

Small cell lung cancer
Gynecologic and breast cancers
Hodgkin lymphoma

241
Q

Paraneoplastic Syndrome: Antibodies against Hu antigens in neurons

A

Small cell lung cancer

242
Q

Paraneoplastic Syndrome: Lambert-Eaton myasthenic syndrome

A

Antibodies against presynaptic Ca2+ channels at NMJ

Small cell lung cancer

243
Q

Paraneoplastic Syndrome: Myasthenia gravis

A

Antibodies against postsynaptic AChR at NMJ

Thymoma

244
Q

Cancer caused by arsenic

A

Liver - angiosarcoma
Lung- lung cancer
Skin - SCC

245
Q

Cancer caused by Aromatic amines

A

Bladder - Transitional cell carcinoma

246
Q

Cancer caused by alkylating agents

A

Blood - leukemia/lymphoma

247
Q

Serum tumor marker: Alkaline phosphatase

A

Mets to bone or liver
Paget disease of one
Seminoma (placental ALP)

248
Q

Serum tumor marker: alpha-fetoprotein

A

Hepatocellular carcioma
Hepatoblastoma
Yolk sac (endodermal sinus) tumor
Mixed germ cell tumor

249
Q

Serum tumor marker: Beta-hCG

A

Hydatidiform moles
Ghoriocarcinomas

(produced by syncytiotrophoblasts of the placenta)

250
Q

Serum tumor marker: CA 15-3/CA 27-29

A

Breast cancer

251
Q

Serum tumor marker: CA 19-9

A

Pancreatic adenocarcinoma

252
Q

Serum tumor marker: CA 125

A

Ovarian cancer

253
Q

Serum tumor marker: Calcitonin

A

Medullary thyroid carcinoma

254
Q

Serum tumor marker: CEA

A

CarcinoEmbyronic Antigen

Very nonspecific, but produced by ~70% of colorectal and pancreatic cancers. Also produced by gastric, breast, and medullary thryoid carcinomas

255
Q

Serum tumor marker: PSA

A

Prostate-specific antigen. Sooooo Prostate cancer.

Can also be elevated in BPH and prostatitis

256
Q

What is P-glycoprotein?

A

aka Multidrug resistance protein 1 (MDR1).
Classically seen in adrenal cell carcinoma but also expressed by colon and liver cancer cells. Used to pump out toxins, including chemotherapeutic agents

257
Q

Cardiac wall damage with LAD infarct

A

Anterior wall

Shared LV/RV wall

258
Q

Cardiac wall damage with RCA infarct

A

Posterior wall

Shared LV/RV wall

259
Q

Cardiac wall damage with L. Circumflex infarct

A

Left lateral wall

260
Q

Systolic Murmurs

A

Aortic Stenosis
Mitral/Tricuspid Regurg
Mitral Valve prolapse
Ventricular septal defect

261
Q

Diastolic Murmurs

A

Aortic regurgitation

Mitral stenosis

262
Q

Murmur heard in Aortic stenosis

A

Systolic

Crescendo-decrescendo systolic ejection murmur (ejection click may be present)
Loudest at heart base. Radiates to carotids
Pulses weak with delayed peak

Can lead to Syncope, Angina, and Dyspnea on exertion

263
Q

Murmur heard in Mitral/Tricuspid Regurgitation

A

Systolic

Holosystolic, high-pitched, “blowing” murmur

Mitral: loudest at apex and radiates to axilla. Often due to ischemia heart disease

Tricuspid: loudest at tricuspid area and radiates to right sternal border. Commonly caused by RV dilatation

264
Q

Murmur heard in Mitral valve Prolapse

A

Systolic

Late systolic crescendo murmur with midsytolic click (due to sudden tensing of chordae tendinae). Most frequent valvular lesion. 
Best heard over apex
Loudest just before S2
Usually benign 
Can predispose to infective endocarditis
265
Q

Murmur heard in Ventricular Septal Defect

A

Holosystolic, harsh-sounding

Loudest at tricuspid area

266
Q

Murmur heard in Aortic Regurgitation

A

Diastolic

High-pitched “blowing” early diastolic decrescendo murmur
Long diastolic murmur
Hyperdynamic pulse, head-bobbing. Wide pulse pressure.
Often due to aortic root dilation, biscupid aortic valve, endocarditis, rheumatic fever.

Progresses to left HF

267
Q

Murmur heard in Mitral Stenosis

A

Diastolic

Follows opening snap
Delayed rumbling late diastolic murmur
Decreased interval between S2 and opening snap correlates with increased severity
LA&raquo_space; LV pressure during diastole

268
Q

Result of Inspiration on cardiac exam

A

Increased venous return of RA

Increases intensity of right heart sounds

269
Q

Result of Hand Grip on cardiac exam

A

Increase in afterload
Increase intensity of MR, AR, VSD murmurs
Decrease in hypertrophic cardiomyopathy murmurs
MVP: later onset of click/murmur

270
Q

Result of Valsalva manuver/Standing up on cardiac exam

A

Decrease preload
Increase intensity of hypertrophic cardiomyopathy murmur
Decrease intensity of most murmurs

271
Q

Result of Rapid Squatting on cardiac exam

A

Increase venous return, Increase preload, Increase afterload

Decrease intensity of hypertorphic cardiomyopaty murmur
Increase in intensity of AS murmur

272
Q

What does S3 heart sound relate to?

A

Associated with increased filling pressure (Mitral regurg, HF)
More common in dilated ventricles
Can be normal in kids and young adults

273
Q

What does S4 heart sound relate to?

A

(Best heart at apex with pt lying on left side)

Associated with ventricular noncompliance (hypertrophy). Left atrium must push against still LV wall.
Always abnormal!

274
Q

What artery supplies the SA and AV nodes?

A

The RCA

275
Q

Conditions when you see an increased pulse pressure

A 
Aortic Regurgitation 
Aortic Stiffening (isolated systolic hypertension in elderly)
Sleep apnea
Exercise
HYPERthyroid
276
Q

Conditions when you see a decreased pulse pressure

A

Aortic stenosis
Cardiogenic shock
Cardiac tamponade
Advanced HF

277
Q

You hear a systolic murmur over the right sternal border. What could it be?

A

Aortic stenosis
Aortic valve sclerosis
Flow murmur (physiologic murmur)

278
Q

You hear a Diastolic murmur over the left sternal border. What could it be?

A

Aortic regurgitation

Pulmonic regurgitation

279
Q

You hear a Systolic murmur over the left sternal border. What could it be?

A

Hypertrophic cardiomyopathy `

280
Q

You hear a Systolic ejection murmur over the pulmonic area. What could it be?

A

Pulmonic stenosis

281
Q

You hear a Holosystolic murmur in the tricuspid area. What could it be?

A

Tricuspid regurgitation

VSD

282
Q

You hear a Diastolic murmur over the tricuspid area. What could it be?

A

Tricuspid stenosis

ASD (increased flow across tricuspid valve)

283
Q

You hear a Holosystolic murmur over the mitral area. What could it be?

A

Mitral regurgitation

284
Q

You hear a Diastolic murmur over the mitral area. What could it be?

A

Mitral stenosis

285
Q

What is Wolff-Parkinson-White syndrome?

A

Most common ventricular pre-excitation syndrome
Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node, so the ventricles start to partially depolarize earlier
See delta wave with widened QRS complex and shortened PR interval

May result in reentry circuit and supraventricular tachycardia

286
Q

What is the “Aldosterone Escape” thing?!

A

A term that has been used to refer to two distinct phenomena involving aldosterone that are exactly opposite each other:

  1. Escape from the sodium-retaining effects of excess aldosterone (or other mineralocorticoids) in primary hyperaldosteronism, manifested by volume and/or pressure natriuresis.
  2. The inability of ACE inhibitor therapy to reliably suppress aldosterone release, for example, in patients with heart failure or diabetes, usually manifested by increased salt and water retention. This latter sense may rather be termed refractory hyperaldosteronism.
287
Q

What the fuck is Phosphodiesterase

A

Any of a class of enzymes that catalyze the hydrolytic cleavage of phosphodiester bonds and are important in breaking down cyclic AMP, cyclic GMP, and nucleic acids

288
Q

What the fuck are Phosphodiesterase Inhibitors and what do they do

A

Well, they inhibit Phosphodiesterase, thereby INCREASING cAMP

Effects: 
Impaire platelet function 
Help you get a boner 
Positive iontropy 
Vasodilation
289
Q

Association to Antibodies to myeloperoxidase and proteinase-3

A

Involved in pathogenesis of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitides such as microscopic polyangiitis and granulomatosis with polyangiitis

290
Q

Association to B-cell activating factor (BAFF)

A

BAFF is a cytokine belonging to the tumor necrosis factor ligand family.

Inadequate levels of BAFF will lead to immunodeficiency

Excess levels cause autoimmune disease

291
Q

DRESS syndrome

A

Rare and potentially life-threatening drug reaction typically occurring 2-8 weeks after exposure to drugs like ANTICONVULSANTS (phenytoin, carbamazepine) ALLOPURINOL, sulfaonamides and some antibiotics (minocyline, vanco).

ESOSINOPHILIA

Presents with fever, generalized lymphadenopathy, facial edema and skin rash

292
Q

Von Recklinghausen’s Disease

A

aka Neurfibromatosis type 1

Inherited peripheral nervous system tumor syndrome. Patients develop neurofibromas, optic nerve gliomas, Lisch nodules (pigmented nodules of the iris), and cafe au lait spots

293
Q

Neurofibromatosis type 2

A

AD

Bilateral cranial nerve VIII schwannomas and multiple meningiomas

294
Q

Sturge-Weber syndrome

A

aka encephalotrigeminal angiomatosis

Congenital neurocutaneous disorder. Cutaneous facial angiomas, leptomeningeal angiomas

Skin involvement typically overlies the ophthalmic (V1) and maxillary (V2) distributions of the trigeminal nerve

Skull shows “tram track” calcifiations

295
Q

Tuberous Sclerosis

A

AD

May cause kideny, liver and pacreatic cysts

CNS hamartomas. Seizures

296
Q

von Hippel-Lindau; Gene and Associated neoplasm

A

VHL gene

Capillary hemangioblastomas in the retina and/or cerebellum. Congenital cysts and/or neoplasms in the kidney, liver and pancreas

Increased risk for renal cell carcinoma, which can be bilateral

297
Q

Lynch syndrome, Genes and Associated neoplasms

A

MSH2
MLH1
MSH6
PMS2

Colorectal cancer
Endometrial cancer
Ovarian cancer

Autosomal Dominant. Caused by inactivating mutation in corresponding tumor suppressor gene (second hit leads to malignant transformation)

298
Q

Familial adenomatous polyposis; Gene and Assocated neoplasms

A

APC

Hemangioblastomas
Clear cell renal cell carincoma
Pheochromocytoma

Autosomal Dominant. Caused by inactivating mutation in corresponding tumor suppressor gene (second hit leads to malignant transformation)

299
Q

Multiple endocrine neoplasia type 1; Gene and Assoicated neoplasms

A

MEN 1

Parathyroid adenomas
Pituitary adenomas
Pancreatic adenomas

Autosomal Dominant. Caused by inactivating mutation in corresponding tumor suppressor gene (second hit leads to malignant transformation)

300
Q

Multiple endocrine neoplasia type 2; Gene and Associated neoplasms

A

RET

Medullary thyroid cancer
Pheochromocytoma
Parathyroid hyperplasia (MEN2A)

Autosomal dominant. ACTIVATING (gain-of-functions)

301
Q

Li-Fraumeni Syndrome; Gene and Associated neoplasms

A

TP53

Sarcomas
Breast cancer
Brain tumors
Adrenocortical carcinoma
Leukemia

Focused Memorization (5 decks)

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