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Green Flags Flashcards

1
Q

active error

A

occurs at level of front line operator- wrong dose programmed in

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2
Q

latent error

A

accident waiting to happen- having various pumps at the hospital

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3
Q

root cause analysis

A

uses records and participant interviews to identify all the underlying problems that led to an error. Prince failure in the future

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4
Q

failure mode and effects analysis

A

uses inductive reasoning to identify all the ways a process might fail and prioritize these by their probability of occurrence and impact on patients

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5
Q

roll over, hands together, laughing

A

3 mo

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6
Q

sit up , transfer cube, single syllables, self feed

A

6 months

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7
Q

crawling, object permanence

A

9 mo

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8
Q

stand/walk, block into cup, 1-3 words, drink from cup

A

12 mo

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9
Q

walk backward, run, build 2 cube tower, 6 words, utensils

A

15 months

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10
Q

stranger anxiety

A

6-12 mo

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11
Q

seperation anxiety

A

12-15 mo

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12
Q

climb stairs, kick ball, 4 cube tower, combine words, brush teeth

A

18 mo

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13
Q

jump 6 cube tower, half understandable, wash and dry hands

A

2yr

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14
Q

jump forward tricycle, copy circle, understandable, pour cereal, brush teeth, dress, play board games

A

3 y

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15
Q

hop on one foot, copy a plus sign draw stick figure, clothes button, magical thinking

A

4y

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16
Q

tie shows, copy square, triangle, identify colors, identify coins, count to five

A

5 yyear

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17
Q

logical thinking

A

6 y

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18
Q

gender identiy

A

3 years

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19
Q

potty train

A

2-3 years

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20
Q

1 std

A

68%

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21
Q

2 std

A

95%

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22
Q

3 std

A

99.7%

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23
Q

cervical LN drain what

A

head and neck

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24
Q

hilar LN drain what

A

lungs

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25
Q

mediastinal LN drain what

A

trachea and esophagus

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26
Q

axillary LN drain what

A

upper limb, breast, skin above the umbilicus

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27
Q

celiac LN drain what

A

liver stomach spleen, pancreas, upper duodenum

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28
Q

SMA LN drain what

A

lower duodenum, jejunum, ileum, colon to the splenic flexure

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29
Q

IMA LN drain what

A

colon from splenic flexure to upper rectum

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30
Q

internal iliac LN drain what

A

lower rectum to anus above the pectinate line, bladder, vagina, cervix, prostate

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31
Q

para-aortic LN drain what

A

testes, ovaries, kidneys, uterus

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32
Q

superficial inguinal LN drain what

A

anus below pectinate line, skin below umbilicus, scrotum, vulva

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33
Q

popliteal LN drain what

A

dorsolateral foot and posterior calf

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34
Q

right lymphatic duct drains what

A

right arm and face above the right diaphragm

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35
Q

thoracic duct drains what

A

everything but the right arm, face and chest drains into the left subclavian

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36
Q

hay fever, rhinitis, eczema, hives, asthma- HSN?

A

HSN1

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37
Q

acute hemolytic transfusion reaction

A

HSN2

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38
Q

bullous pemphigoid

A

HSN2

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39
Q

anaphyalxis

A

HS1

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40
Q

autoimmune hemolytic anemia

A

HSN2

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41
Q

SLE

A

HSN3

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42
Q

contact dermatitis

A

HSN4

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43
Q

Graft vs host

A

HSN4

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44
Q

MS

A

HSN4

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45
Q

polyarteritis nodosa

A

HSN3

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46
Q

myasthenia gravis

A

HSN2

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47
Q

goodpasture

A

HSN2

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48
Q

Graves

A

HSN2

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49
Q

GBS

A

HSN2

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50
Q

poststep glomerulonephritis

A

HSN3

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51
Q

serum sickness

A

HSN3

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52
Q

ITP

A

HSN2

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53
Q

MG

A

HSN2

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54
Q

pemphigus vulgaris

A

HSN2

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55
Q

Rheumatic fever

A

HSN2

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56
Q

type 3 HSN

A

immune complex deposition which activates complement which attracts neutrophils and these release lysosomal enzymes. Can have vasculitis and systemic manifestations

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57
Q

serum sickness

A

an HSN3 where antibodies to foreign protein are produces and immune complezes deposit and they fix complement

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58
Q

arthus reaction

A

local subacture antibody mediated HSN reaction. INtradermal injection of antigen presented individual leads to complex formation in the skin leading to edema, necrosis, and activation of complement

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59
Q

type IV HSN

A

delayed T cell mediated response when sensitized T cells encounter the antigen then they release cytokines. This leads to macrophage activation.

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60
Q

what is the candidal skin test test? what if there is no response to it

A

HSN4 and have SCID

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61
Q

anti-Ach receptor

A

Myasthenia gravis

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62
Q

Anti basement membrane

A

goodpasture

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63
Q

anticadiolipin

A

SLE

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64
Q

anticentromere

A

CRESt

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65
Q

anti-desmoglein

A

pemphigous vulgaris

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66
Q

anti-dsDNA and anti-smith

A

SLE

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67
Q

anti-glutamic acid decarboxylase

A

type 1 DM

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68
Q

antihemidesmosome

A

bullous pemphigoid

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69
Q

antihistone

A

drug induced lupus

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70
Q

anti-jo-1, anti SRP, anti mi-2

A

polymyositis, and dermatomyositis

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71
Q

antimicrosomal, antithyroglobulin

A

hashimoto

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72
Q

antimitochondrial

A

primary billiary cirrohsis

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73
Q

antinuclear

A

SLE

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74
Q

antiparietal cell

A

pernicious anemia

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75
Q

antiphospholipase A2 receptor

A

primary membranous nephropathy

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76
Q

Anti-Scl70 anti DNA toposiomerase

A

Scleroderma- diffuse

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77
Q

antismooth muscle

A

autoimmune hepatitis

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78
Q

anti SSA anti SSB- anti Ro and La

A

Sjogren syndrome

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79
Q

anti TSh receptor

A

graves disease

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80
Q

anti-U1 RNP

A

mixed CT disorder

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81
Q

voltage gated CCB antibodies

A

Lambert Eaton

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82
Q

IgA antiendomyseal and anti tissue transglutaminase

A

Celiac disease

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83
Q

MPO anca/ panca

A

microscopic polyangiatis, eosinophilic granulomatosis with polyangiitis- Churgg Strauss

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84
Q

PR3-anca or cANCA

A

granulomatosis with polyangiitis-Wegner

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85
Q

Rheumatoid factor and anti-CCP

A

rhematiod arthritis

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86
Q

APC

A

colon cancer

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87
Q

BRCA1

A

breast cancer- DNA repair protein

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88
Q

CDKN2A

A

melanoma and pancreatic cancer- blocks G1- S phase

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89
Q

DCC

A

colon cancer

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90
Q

DPC4/SMAD4

A

pancreatic cancer

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91
Q

MEN1

A

menin- MEN1

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92
Q

NF1

A

RAS gtapse

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93
Q

NF2

A

merlin protein

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94
Q

PTEN

A

breast cancer, prostate cancer, endometrial cancer

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95
Q

Rb

A

retinoblastoma and osteosarcoma- blocks G1 to S phase

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96
Q

P53

A

Li fraumani or otehr cancers- activates p2 and regulates g1 to S and G2 to M

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97
Q

TSC1

A

hamartin protein- tuberous sclerosis

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98
Q

TSC2

A

tuberin protein- tuberous sclerosis

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99
Q

VHL

A

VHL and RCC- inhibits hypoxia inducible factor Ia

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100
Q

WT1/WT2

A

wilms tumor

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101
Q

alkaline phsophatase

A

metastasis to bone or liver- paget of bones

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102
Q

alpha fetoprotein

A

hepatocellular cacrincoma, hepatoblastoma, yolk sac tumor, mized germ cell tumor- high in NT defects

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103
Q

CA15-3/Ca27-29

A

breast cancer

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104
Q

CA19-9

A

pancreatic cancer

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105
Q

CA 125

A

ovarian cancer

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106
Q

calcitonin

A

medullary thyroid carcinoma

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107
Q

CEA

A

increased in pancreatic or colon cancer- produced by gastric, breast, and thyroid

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108
Q

PSA

A

only specific to prostate pathology

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109
Q

p-glycoprotein

A

adrenal cell carcinoma but the cancers that can pump chemo out of the cell

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110
Q

cachexia what factors mediate it

A

mediated by TNF, IFN gamma, and IL1 and 6

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111
Q

what mets to the brain

A

lung, breast, prostate, melanoma, GI

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112
Q

what mets to the liver

A

colon, stomach, pancreas

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113
Q

what mets to the bone and is blastic

A

prostate, testes

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114
Q

what mets to the bone and are lytic

A

rental cell, thyroid

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115
Q

what mets to the bone and are blastic and lytic

A

lung, breast

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116
Q

site of synthesis of secretory exported proteins and of N linked oligosaccharide addition to many proteins. It is in the nil bodies to synthesize the peptide NT and free ribosimes are there to synthesize proteins in the sytoplasm. Goblet cells and plasma cells have an increased proportion of this organelle

A

Rough Er

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117
Q

site of steroid synthesis and detox of drugs and poisons. These are in the hepatocytes and steroid hormone producing cells of the adrenal cortex and gonads- which organelle is this

A

Smooth Er

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118
Q

distribution center for proteins and lipids form the ER to the visible and plasma membranes. Ads oligosaccharides and mannose 6 phosphate- what organelle is this

A

golgi body

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119
Q

coarse facial features, cloudy corneas, restricted joints, and high plasma levels of lysosomal enzymes. often have fatal in childhood- what is failing here

A

there is no mannose 6 phosphate to lysosomal enzymes are secreted instead of directed to the lysosomes

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120
Q

COP1 does which direction of transport

A

golgi to ribosome

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121
Q

COPII is which direction of transport

A

ribosome to golgi

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122
Q

what does a peroxisome do

A

catabolism of very long chain fatty acids, fatty acids, and amino acids and ethanol- it also produces a part of the myelin

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123
Q

what does a proteasome do

A

degrade damaged or ubiquitinated proteins

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124
Q

carrier frequency equation

A

2squareroot(disease prevalence)

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125
Q

the frequency of X linked disease in males and females according to hardy weinburg

A

males=q and females=Qsquared

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126
Q

when does hardy weinburg numbers do not work

A

linkage dis-equalibrim means that these are stuck together which leads differences in the ratio

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127
Q

hardy weinburg eqn

A

psquared+2pq+qsquared: p is homozygois and pQ are heterozygotes

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128
Q

effect male and females of each generation

A

autosomal dominant

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129
Q

tend to be more severe disorder and is in only 1 generation overall- if there are two carrier parents then there will be 25% chance of being effected

A

autosomal recessive

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130
Q

more severe in males, and there is a 50% chance of being affected if male- skips generations

A

X-linked recessive

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131
Q

transmitted through either parent- 50% of daughters and sons, fathers transmit to all daughters-

A

X linked dominant

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132
Q

inheritted disorder of increased phosphate wasting at proximal tubules and resultless in rickets- what is it called

A

hypophosphatemic rickets

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133
Q

myopathy, lactic acidosis, CNS disease, stroke like episodes, and failure of oxidative phosphorylation and ragged red fibers

A

mitochondrial myopathies- transmitted through the mother

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134
Q

mutation in FGF3 inhibits chondrocyte prolideration. It presents as dwarfism

A

achondroplasia

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135
Q

what is the enzyme deficient in albinism

A

tyrosinase

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136
Q

intellectual disability, growth retardation, seizures, fair skin, eczema, musty body odor– what is deficient, what is the treatment, and what aa is bad

A

due to decreased phenylalanine hydroxylase or tetrahydrobiopterin cofactor- tyrosine is essential because increased phenylalanine is toxic. Treatment is to increase tyrosine in the diet and tetrahydrobiopterin and to decrease PK.

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137
Q

what looks different if tetrahydrobiopterin is deficient in PKU

A

can have increased prolactin and decreased NE. Can have an increased phenylalanine and decreased serotonin.

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138
Q

what are the maternal effects of PKU

A

child will have microcephaly, disability, and heart defects

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139
Q

patient has pancreatitis, hepatosplenomegaly, and erupt pruritic xanthomas and a creamy layer of blood- what is the defect, what are the risks associated, and what are the increased blood levels

A

lipoprotin lipase of ApoC2 def- no increased risk for atheroscelsis- test with hepatic to see LPL activity and body can’t clear the dietary lipids- hyperchylomicronemia- AR

140
Q

patient have 700+cholesterol, and accerleared atheroscelosis, tendon xanthomas, and corneal arcus-what is the defect, what are the risks associated, and what are the increased blood levels

A

familial hypercholesterolemia-AD- increased LDL and cholesterol for missing LDL receptors

141
Q

patient has massive increase in TG which can cause acute pancreatitis-what is the defect, what are the risks associated, and what are the increased blood levels

A

hyper TG- AD- hepatic overproduction of VLDL

142
Q

steatorrhea and liked red blood cells, ataxia, nightblindness-what is the defect, what are the risks associated, and what are the increased blood levels

A

decreased APOB48- AR so there is a decreased in apoB100 and a mutation in MTP this leads to decreased VLDL and chylomicrons so increased TAG in enterocytes- cannot get rid of the TAGS- abetalipoproteinmia

143
Q

pharyngitis with pseudomembranes in the throat and sever lymphadenopathy- inactive the elongation factor 2- what is the toxin and disease

A

diptheria toxin

144
Q

inactives elongation factor EF2- what is the toxin and disease

A

exotoxin a from pseudomanas

145
Q

inactivates 6- s ribosome from removing adenine from the rRNA- G mucosal damage and dysentary, can cause hemolytic uremic syndrome- what is the toxin and disease

A

shiga toxin- shigella

146
Q

enhances cytokine release causing HUS and it inactivates the 60S ribosome by removing adenine from rRNA- what is the toxin and disease

A

Shia like toxin- EHEC O157H7

147
Q

over activates the adenylate cyclase to increase cAMP and increase Cl secretion in the gut and H2O effulx watery diarrhea- what is the toxin and disease- what is the toxin and disease

A

heat labile LT in ETEC

148
Q

over activation of guanylate cyclase and increase cGMP and decrease responion of Nacl and H2O in the gut. leading to watery diarrhea - what is the toxin and disease

A

heat stable ETEC

149
Q

mimics the adenylate cyclase enzyme and increased cAMP- edema on the edges on tan eschar- what is the toxin and disease

A

edema toxin of bacillus anthracis

150
Q

overactivates adenylate cyclase and increase cAMP by permanently activating Gs in the gut and increases the Cl secretion in the gut and water effflux- leas to voluminous rice water stools with increased infection in people with decreased gastric acid- what is the toxin and disease

A

cholera toxin

151
Q

child coughs on expiration and whoops on inspiration- over activation of adenylate cyclase and this increases cAMP and disables Gi by impairing phagocytosis to permit survival- what is the toxin and disease

A

pertisus toxin

152
Q

protease that cleaves the SNARE protein and it is required for normal NT release from vesicular fusion- spastic paralysis with rises sardonic and lockjaw and prevents release of inhibitory NT from the Renshaw cells- what is the toxin and disease

A

tetanospasmin- clostridium tetani

153
Q

protease that cleaves SNARE protein and it is required for NT release from vesicular fusion- flaccid paralysis, floppy babe, toxin prevents release of stimulatory ACH signals from NMJ, can have diplopia, dysphagia, and respiratory depression- what is the toxin and disease

A

clostridium botulinum-

154
Q

phospholipase that degrades tissue and cell membranes- degradation of phospholipids leading to a double zone of hemolysis on blood agar and myonecrosis- what is the toxin and disease

A

alpha toxin- perfringins

155
Q

protein that degrades cell membanes- lyses RBC and contributes to beta hemolysis- used to diagnose rheumatic fever streptolysin O- what is the toxin and disease

A

strep pyogenes- streptolysin O

156
Q

inhibits activation of complement and phagocytosis- what is the toxin and disease

A

strep pyogenes- protein M

157
Q

binds to MHCII and TCR causing oerwelming release of IL1,IL2,IFNgamma, TNFalpha- shock- fever, rash, and rash

A

toxic shock syndome in s.aureus and exotoxin A in strep pyogenes

158
Q

which staph is novobiocin resistant

A

saprophyticus

159
Q

which staph is novobiocin sensitive

A

epidermidis

160
Q

optochin sensitive

A

strep pneumo

161
Q

optochin resistant

A

strep vidians

162
Q

headache, nonproductive cough, patchy or diffuse interstitial infiltrate and X ray looks bad- positive cold agglutination test and can lyse RBC. Not seen on grab stain frequently in young college or military recruits

A

mycoplasma pneumoniae

163
Q

what does mycoplasma have in its cell wall

A

sterols for stability

164
Q

what are the CSF findings in bacterial meningitis

A

increased neutrophils, increased protein, decreased glucose

165
Q

what are the CSF findings in fungal/TB meningitis

A

increased lymphocytes, increased protein, decreased glucose

166
Q

what are the CSF findings in viral meningitis

A

increased lymphocytes, normal to increased protein and normal sugar

167
Q

what is the function of alpha1 and what Gprotein are they with

A

Gq- increased vascular smooth muscle contraction, increased pupillary contraction, increased in intestinal and bladder sphincter muscle tone

168
Q

what is the function of alpha2 and what Gprotein are they with

A

Gi- decreased sympathetic outflow and decreased insulin release, decreased lipolysis, increased platelet aggregation, decreased aqueous humor production

169
Q

what is the function of beta1 and what Gprotein are they with

A

Gs- increased heart rate, increased contractility, increased renin release, increased lipolysis

170
Q

what is the function of beta2 and what Gprotein are they with

A

Gs- vasodilation, bronchodilatiion, increased lipolysis, increased insulin release, decreased uterine tone, cilary muscle relaxation, increased aqueous humor production

171
Q

what is the function of beta3 and what Gprotein are they with

A

Gs- increased lipolysis, increased thermogenesis in skeletal muscle

172
Q

what is the function of M1 and what Gprotein are they with

A

Gq- CNS and enteric nervous system- stomach

173
Q

what is the function of M2 and what Gprotein are they with

A

Gi- decreased heart rate and contractility of the atria

174
Q

what is the function of M3 and what Gprotein are they with

A

Gq- increased exocrine gland secretion, lacrimal, sweat, salivary, gastric acid, increased gut peristalsis, increased bladder contraction, bronchoconstriction, increased pupil contraction, mitosis and accomidation

175
Q

what is the function of D1 and what Gprotein are they with

A

Gs- relaxes renal vascular smooth muscle

176
Q

what is the function of D2 and what Gprotein are they with

A

Gi- modulated tranmitter release in the brain

177
Q

dopamine given at a low dose leads to what

A

increased heart contraction and increased renal blood flow

178
Q

what is the function of H1 and what Gprotein are they with

A

Gq- increased nasal and bronchial mucus production, increased vascular permeability, increased contraction of bronchioles, increased parities and pain

179
Q

what is the function of H2 and what Gprotein are they with

A

Gs- increased gastric acid secretion

180
Q

what is the function of V1 and what Gprotein are they with

A

Gq- increased vascular smooth muscle contraction like pressers it increases the BP and it increases from constriction

181
Q

what is the function of V2 and what Gprotein are they with

A

Gs- it increases H2O permeability and reabsorption in collecting tubules of the kidneys

182
Q

what are controlled by Gq

A

H1, a1, v1, M1, M3

183
Q

what are controlled by Gs

A

B1, B2, B3, D1, H2,V2

184
Q

what are controlled Gi

A

M2, a2, D2

185
Q

what connects the tongue to the thyroid in embryonic development- what is the remnant called and what is the embryonic structure called

A

It is the thyroglossal duct and if it persists it forms the pyramidal lobe of the thyroid

186
Q

where can ectopic thyroid tissue be found and what are the complications if its removed

A

its called a lingual thyroid and it can lead to hypothyroid if it is the only thyroid tissue present

187
Q

what is a midline neck mass that moves with swallow or protrusion of the tongue

A

it is a thyroglossal duct cyst

188
Q

what is a lateral neck mass that does not move with swallow

A

branchial cleft cyst

189
Q

what is the embryonic origin of thyroid tissue and which cells are derived from something different

A

thyroid is from the endoderm and the parafollicular cells are from neural crest

190
Q

what is the adrenal cortex derived from and what is the adrenal medulla derived from

A

the cortex is from the mesoderm and the medulla is from the neural crest cells

191
Q

Cushing syndrome- what can cause it

A
  • exogenous steroids- leads to bilateral adrenal atrophy
  • primary adrenal adnoma, hyperplasia, or carcinoma- leads to decreased ACTH and increased cortisol- only one large on
  • acth pituitary adenoma- increased ACTH so bilateral hypertrophy
192
Q

findings with Cushing

A

HTN, moon face, striae, tunnel obesity, buffalo hump, osteoporosis, hyperglycemia, amenorrhea, immunosuppression

193
Q

how to diagnose- what is the dexamethasone suppression test

A

no suppression if its ectopic. Only suppressed if it is from an acth adenoma of the pituitary

194
Q

diabetic ketoacidosis

A

usually due to insulin noncompliance, increased insulin requirements from stress, excess fat breakdown and increased ketogenesis from increased free fatty acids, which are the name into ketone bodies, Beta hydroxybutarate is increased over acetoacetate. Usually occurs n DM1, as endogenous insulin in DM 2, and prevents lipolysis

195
Q

signs of DKA

A

delirium, psychosis, Kussmal breathing (deep/rapid breathing), abdominal pain/nausea/vomiting, dehydration, fruity breath odor

196
Q

labs for DKA

A

hyperglycemia, increased H decreased bicarb, ADMA increased ketones, leukocytosis. hyperkalemia but depleted intracellular K due to transcellualr shift from decreased insulin

197
Q

complications of DKA

A

mucomycosis or rhizopus, cerebral edma, cardiac arrhythmias, heart failure

198
Q

treat of DKA

A

IV fluids, insulin, K to replete intracellular stores

199
Q

hyperosmolar hyperglycemia nonkeotic syndrome

A

state of profound hyperglycemia induced dehydration and increased serum osmolality, seen in elderly with DM 2 with limited ability to drink. Hyperglycemia and excessive osmotic diuresis, dehydration, eventual one of this. Thirst, polyuria, leathery, focal neurological defects, and coma if left untreated

200
Q

labs of hyperosmolar hyperglycemic nonketotic syndrome

A

increased serum osmolality, hyerpglycemia, no acidosis because the ketone production is inhibited by insulin.

201
Q

treatment of hyperosmolar hyperglycemia nonketotic syndrome

A

aggressive IV fluids, insulin therapy

202
Q

what are the first treatment strategies of type 1 DM

A

low carb diet, insulin replacement

203
Q

what are the first treatment strategies of type 2 DM

A

diet modification, exercise, insulin replacement if lifestyle modification fails

204
Q

which are the rapid acting insulins

A

lispro, aspart, glulisine- no LAG

205
Q

MOA of insulin

A

binds the insulin receptor and increases the tyrosine kinase activity quickly. liver increases the glucose stores as glycogen, and increase the glycogen protein synthesis and K uptake, increase TG storage

206
Q

side effects of insulin

A

hypoglycemia, lipodystrophy, some hypersensitivity reactions

207
Q

short acting insulin

A

regular insulin

208
Q

intermediate insulin

A

NPH insulin

209
Q

long acting insulin

A

detemir, glargine used for basal control of diabetes

210
Q

metformin what does it do

A

decreased gluconeogenesis, increase glycolysis, increase peripheral glucose uptake, increased insulin sensitivity

211
Q

metformin clincial use

A

first line with some modest weight loss, can be used in patients with no islet function.

212
Q

metformin risks and ocncerns

A

GI upset, lactic acidosis in people with renal insufficiency

213
Q

sulfonylureas- names

A

chloropropamide, tolbutamide, glimepriride, glipizide, glyburide

214
Q

sulfonylureas- MOA

A

close the K channel in the beta cell which causes the increase release of insulin from depolarization and ca influx.

215
Q

sulfonylurea clinical use

A

stimulater release of endogenous insulin require some islet cell function.

216
Q

sulfonylureas- risks and concerns

A

risk of hypoglycemia increased in exercise, missed meals, malnourishment, organ dysfunction, risk is increased in renal failure. there is weight gain. Can have disulfiram reaction, and hypoglycemia

217
Q

glitazones/thiazolidinediones- MOA

A

increased insulin sensitivity in peripheral tissue bids to PPAR gamma nuclear transcription regulator- it is inranuclear receptor that acts as transcriptional regulator. PPAR is a transcription regulator which decreases the receptors

218
Q

glitazones/thiazolidinediones- clinical use

A

good for people with renal impairment

219
Q

glitazones/thiazolidinediones- side effects

A

weight gain, edema, flood retention from increased NA reabsorption in CT. can lead to increase adipose and exacerbation of HF, also hepatotoxic and increased risk of fractures

220
Q

meglitinides- which ones

A

nateglinide, and repaglinide

221
Q

meglitinides- MOA

A

stimualte postprandial insulin release by binding to k channels on beta cell membranes

222
Q

meglitinides- clinical use

A

mono therapy in DM 2 or combined with metformin

223
Q

meglitinides- side effects

A

hypoglycemia increased risk with renal failure see weight gain

224
Q

GLP1 analogs- which

A

exantide, liraglutide

225
Q

GLP1 analogs- MOA

A

increase glucose dependent insulin release, decreased glucagon secretion, decreased gastric emptying, increased satiety

226
Q

GLP1 analogs- side effects

A

nausea, vomiting, pancreatitis, modest weight loss

227
Q

DDP4 inhibitors- which

228
Q

DDP4 inhibitors- MOA

A

inhibits DPP4 enzyme that activities GLP1 increased glucose dependent insulin release, decrease glucagon release, decreased gastric emptying, increased satiety

229
Q

DDP4 inhibitors- side effects

A

mild urinary or respiratory infections

230
Q

amylin analogs- which

A

pramlintide

231
Q

amylin analogs- MOA

A

decreased gastric emptying, decreased glucagon

232
Q

amylin analogs- side effects

A

hypoglycemia in the setting of mistimed prandial insulin, and nausea

233
Q

SGLT2 inhibitors- which

234
Q

SGLT2 inhibitors- MOA

A

block resorption of glucose at the PCT

235
Q

SGLT2 inhibitors- side effects

A

avoid with bad kidneys have to look at the Cr and BUN before starting- glucosauria, UTI, vaginal yeast infections, hyperkalemia, dehydration, orthostatic hypotension

236
Q

alpha glucosidase inhibitors- which

A

acarbose, miglitol

237
Q

alpha glucosidase inhibitors- MOA

A

inhibit intestinal brush border aha glucosidases. delayed carbohydrate hydrolysis and glucose absorption. decreased postprandial hyperglycemia

238
Q

flip through some abdominal CT

239
Q

what supplies the lower esophagus to proximal duodenum- artery and nerve

A

celiac artery and vagus nerve

240
Q

what supplies the distal duodenum to proximal 2/3 of the transverse colon- artery and nerve

A

SMA and vagus

241
Q

what supplies the distal 1/3 of the transverse colon to the upper portion of the rectum- artery and nerve

A

IMA and pelvic

242
Q

celiac disease

A

gluten sensitive enteropathy, celiac sprue- autoimmune mediated intolerance of gladian- malabsorption and steatorrhea. Associated with HLA-DQ2 DQ8, northern european descent, dermatitis herpetiformis, decreased bone density. IgA anti-tissue transglutaminase, anti-endomysial, antk-deamindated gliadin peptide antibodies- villous atrophy and crypt hyperplasia with intraepithelial lymphocytosis. increased malignancy- short stature, blasting, diarrhea, and fart, weight loss

243
Q

what is the sudan stain used for

A

fats are first so this is high confidence of malsoprtion

244
Q

Crohn

A

skip lesions, rectal sparing, cobblesteone mucosa, creeping fat, bowel wall thickening, noncaseating granluomas and lymphoid aggregates, malabsorption malnutrition, colorectal cancer, increased risk punctilios, abscess/strictures, perianal disease- diarrhea that may or not be bloody. Rash, arteritis, ulcerations. Kidney stones, gallstones- treatment of corticosteroids,

245
Q

what kind of kidney stones does crohns get

A

calcium oxalate because of decreased calcium oxalate binding

246
Q

treatment of crohns

A

corticosteroids, azothioprine, antibiotics like ciprofloxacin, metronidazole, infliximab, adailimumab

247
Q

untreated healing crohns has what cytokine present

A

IL10 which decreases the Th1 activities and the Th1 tends to causes the granulomas

248
Q

ulcrative colitits

A

ulcers, large intestein, continuous, oclorectal canceer, crypt abscesses, extends proimally, red diarrhea, scelrosis cholangitis. pANCe

249
Q

toxic megacolon symptoms

A

abdominal pain, fever, air fluid levels, shock, bloody diarrhea, perforation

250
Q

what are the extra intestinal manifestations of inflammatory bowel disease

A

rash, eye inflammation, oral ulcerations, arthritis

251
Q

treatment of UC

A

5-aminosalicylac preparations, 6-mercaptopurine, infliximab, colectomy

252
Q

cancer from IBD looks like

A

younger with flat and non, polyps with signet rings cells early p53 mutations and late APC, proximal colon, multifocal usually 10 years after UC

253
Q

irritable bowel syndrom

A

recurrnt abdominal pain with pain that improves with defectation, change in stool frequency, change in appearance of stool- middle ages women

254
Q

hemispatial neglect- where is the lesion

A

nondominant parietal cortex

255
Q

agraphia, aculculia, finger agnosia, left right disorientation- where is the lesion

A

dominant parietal cortex

256
Q

CN III damage motor output

A

it is to the ocular muscles- affected primarily by vascular disease and due to decreased diffusion of oxygen and nutrients to the interior firbers from compromised vascular that resides on the outdoes of the nerve. ptosis and down and out gaze

257
Q

what is the parasympathetic output to the CNIII

A

it is fibers on the peripheray and its first from compression so the sings are diminished or absent pupillary reflex and blown pupil with down and out

258
Q

diabetic CNIII damage-

A

acute diplopia, down and out from ischemic damage which is at the core then spreads out. The size is normaal-acute has to be down and out first then it can start getting some reactivity

259
Q

compression of CNIII

A

peripheral is first from the parasympathetic firsts on the outside being compress so there is effect in reactivity to light and its down and out. Typically from posterior communicating and then it can be from uncal herniation

260
Q

CN IV dmage

A

eyes move upward with contralateral gaze so tilt head towards the eyes of the lesion

261
Q

how can a CN IV lesion present

A

it can present with compensatory head tilt and trouble going down stairs

262
Q

CN VI palsy

A

cannot abduct the eye so it cannot move out

263
Q

what is the lesion from if you can only see out of one eye

A

right anopia- optic nerve lesion

264
Q

what if you can’t see the temporal sides of your vision

A

bitemporal hemianopsia- so have something compressing the optic chiasm like a pituitary adenoma or craniopharyngeoma

265
Q

what if you can only see the left parts of your vision

A

the lesion is at the optic tract and its homonymous hemianopia

266
Q

what if you can only see the top quarter of both eyes- pie in the sky

A

right temporal lesion of MCA- and its from meyers loop

267
Q

what if you can only see the bottom quarter of both eyes- pie on the floor

A

Right pariteal lesion or MCA- its opposite from the side of lesion

268
Q

hemianopia with macular sparing

A

PCA infact

269
Q

entral scotoma

A

only lose the middle of the middle-

270
Q

draw the brachial plexus and write out the order of the things

A

did you actually do it?

271
Q

RA pathogenesis

A

infalmmatory cytokines and cells induce a pannus formation with proliferative fraunaltio information which erodes the cartilage and bone

272
Q

RA predisposing facotrs

A

female, HLDR4, and smoking, and silica exposure.

273
Q

what is the more specific test for Ra

A

it is anti-cyclic citrullinated peptide antibody

274
Q

presnsetation of RA

A

pain, swelling, morning stiffness, lasting under 1 hour. symmetric joint inclement with fever and fatigure

275
Q

what test should you get for RA regularly

A

cervical XR to check for subluxation.

276
Q

what joints of the hands does RA not involve

A

it does not idled the DIP

277
Q

what are the treatments for RA

A

NSAIDs, and methotrexate and sulfasalazine, hydroxychrlorowine, leflunomide, TNF alpha inhibitors

278
Q

what can subluxation lead to and what would the symptoms be RA

A

it is from increased risk of RA and incubation and lead to spinal compression and flaccid paralysis

279
Q

sarcoidosis

A

widespread noncaseating granulomas- elected ACE, and elevated CD4/CD8- bilateral adenopathy and coarse reticular opacities. Extensive hailer and mediastinal adenopathy. It is associated with restrictive long disease, and erythema podium, lupus perinea on skin, and bell palsy, epithelium granulomas, uveitis, hypercalcemia. increased 1 alpha hydroxylate mediated vitamin D activation.

280
Q

what cytokines are active in sarcoid

A

it is Th1 and iL2 and IFN gamma increased so macrophages to granulam

281
Q

what are the lab levels of calcium and vitamin D for sarcoidoisis

A

increased 1,5 vitamin D, decreased PTH and increased Ca

282
Q

arachadonic acid path

283
Q

what does airway obstruction lead to in terms of values

A

decreased FVC, decreased FEV1, decreased ration, and increased TLC

284
Q

Chronic bronchitis presentation

A

it is 3 months over 2 years from smoking large areas. It is glandualr hyperplasia leading to increased mucus which forms plus and then leads to cough and increased PaCO2 and decreased PaO2, and

285
Q

chronic bronchitis complications

A

increased risk of infections and for pulmonate, clamp down to shunt from O2 low region and move it to other areas, but if its all over from disease all over can create increased RH work which led to right heart hypertrophy and failure.

286
Q

emphysema presentation

A

destroy alveolar sacs from exchange so increased collapse because cant have enough elastic roil to stay open. It is dyspnea, airway collapse of small ones, purse lips for increased back pressure to prevent trapping, and pink offer ,weight loss from increased breathing work ,and wide chest from increased chest pull out

287
Q

what is emphysema pathophysiology of smoking caused

A

centracinar emphysema- it is increased proteases because of the extra inflammation which is more than the alpha 1 can handle

288
Q

what is the pathophysiology of alpha 1 antitrypsin

A

it is no protection from protease damage because too much proteases. It is panacean emphysema and lower lobe pneumonia get cirrhosis from misfolded protein build up in the hepatocytes and this causes pink PAS positive globules. these are in the endoplasmic reticulum

289
Q

what is the gene for alpha 1 anti-trypsin and what is the difference with a heterozygote and homozygote

A

-PiM is normal allele and the common mutation is PiZ. If you are homozygous, you will get it. There is PiZ and PiM together then it is you are heterozygous so should not smoke, but need to keep lungs protected because some increased risk from decreased production,

290
Q

what are the cytokines that induce asthma

A

TH2, IL4-IgE, IL5-eosinophils, IL10- inhibit Th1, and so increased Th2

291
Q

pathophysiology of asthma

A

it is re-exposure causes cross linking of IgE and this activates mast cells and dump histamine and causes vasodilation,in venues and it causes fluid from posterior capillary venues. Leukotriene C4, D4,E4- constriction and inflammation leads to bronchoconstriciton and perpetuats the constriction.

292
Q

bronchiectaasis

A

abnormal dilated airways - lose tone and air trapping whorls because the air can’t get out. Large airspaces and necrotizing inflammation and damage to the wall

293
Q

who gets bronchiectasis

A

CF (thick sputum), Kartageners (dynein arm less movement), tumor or foreign body, necrotizing infection like Kleb, and allergic bronchopulmonary aspergillum (asthmatics or CF gets HSN reactions to aspergillum.

294
Q

what are the complications of bronchiectasis

A

hypoxia and cor pulmonale, and secondary amyloidosis

295
Q

foul smelling sputum, dyspnea, cough

A

bronchiectasis

296
Q

what is the differential for digital clubbing

A

bronchiextasis, large cell lung cancer, TB, CF, empyema, chronic lung abscess

297
Q

what are charcot leyden crystals

A

they are esonophilic crystals from breakdown of eosinophils in the sputum (bmp)

298
Q

what cell type leads to the emphysema seen in smokers

A

activation of macrophages of neutrophils and macrophages to damage and increased proteases and decrease antiprotease activity

299
Q

what are the benign lung lesions and what can cause them

A

benign hamartomas and grnulomas (histoplasma and TB)

300
Q

what is the bad part of cigarette smoke causing cancer

A

polycyclic aromatic hydrocarbons

301
Q

what do you look for if there is a mass on lesion on the lung

A

look at old XR to see if anything has changed

302
Q

what are hamartomas composed of

A

calcified on imaging and has cartilage and lung tissue

303
Q

small cell lung cancer what does it look like

A

poor differentiated small cells, central tumor on smokers and increased mitosis

304
Q

small cell lung cancer: what are the paraneoplastic syndromes

A

ADH, ACTH, and Lambert Eaton (presynaptic calcium channels)

305
Q

squamous cell carcinoma histology

A

keratin pearls and intracellular bridges which are desmosomal connections

306
Q

where is the squamous cell tumor and what are the paraneoplastic syndromes

A

PTHrP and increased Ca, and central tumor of male smokers

307
Q

large cell tumor histology

A

poor differentiation with poor prognosis

308
Q

bronchioloalveloar tumor

A

tumor on small airway and malignant Clara cells and peripheral looks like pneumonia and walls of alveoli are replaced by tall columnar cells

309
Q

carcinoid tumors

A

neuroendocrine tumors and polyp mass on the bronchi positive chromogranin

310
Q

what cancer is involved or moves to the pleura

A

adenocarcinoma

311
Q

what are some of the complications of lung cancer

A

pleural involvement (adenocarcinoma), obstruction of the SVC, phrenic or laryngeal nerve, pan coast tumor (pinpoint pupil, and anhidrosis of the forehead , and ptosis

312
Q

where does a lung tumor met to

A

adrenal glands

313
Q

what are the things associated with potter sequence or syndrome

A

pulmonary hypoplasai, oligohydramnios, twisted face, twistedd skin, extremity defects, renal failures in utero

314
Q

what are the causes of potter sequence

A

ARPKD (small cysts on kidneys in utero), obstructive uropathy (prosterior urethral valvees), bilateral renal agenesis, chronic placental insufficiency

315
Q

what poles of the kidneys fuse on horseshoe kidney

A

it is inferior poles that are fused.

316
Q

what does the horseshoe kidney get stuck on

317
Q

what are horseshoe kidneys associated with

A

hydronephrosis, renal stones, infection, chromosomal aneuploidy and sometimes cancer

318
Q

neural crest derivatives

A

melanocytes, aorticopulmonary septum, ganglia, irirs, chromaffin cells, cranial nerves, odontoblasts, ossibles, parafollicular cells, sclera

319
Q

what is the male formation like from the internal and external path

A

SRY end turns on testis determining factor and it hits the testes and increases the serotli cells

  • internal - settle cells secrete mullein inhibitory factor and this degenerates the paramesonephric ducts
  • external- the leydig cells are stimulates to secrete testosterone and this cause the wolfing duct to develop which is the internal structures like the everything but the prostate. It then converts to DHT and this is what starts the male external genitalkia
320
Q

what happens if there are no sertoli cells or they lack MIF

A

develop male and female internal genitalia and male external genitalia

321
Q

what happens if 5 alpha reductase is deficitnet

A

inability to convert t to DHT causes male internal genitalia nbut ambigious on the outside- Dominican children that sprout penises at puberty.

322
Q

Paramesoneprhic development

A

no SRY gene, so it develops into female internal structures, fallopian tubes, uterus, upper portion of the vagina

323
Q

what happens for mullein agensis

A

may present as primary amenorrhea due to lack of uterus with females with full functional ovaries and secondary sexual chaaracterisics

324
Q

what is the homolog of glans penis

325
Q

what is the homolog of crops vavernosu man spongiosum

A

vestibular bulbs

326
Q

what is the homolog of bulbourethral glands

A

greater vestibular glands

327
Q

what is the homolog of prostate gland

A

urethral and parauterthal glands

328
Q

what is the homolog of ventral shaft of the penis

A

labia minora

329
Q

what is the homolog of scrotum

A

labia majora

330
Q

hypospadia

A

the opening is on the bottom and its the failure of the urethral folds

331
Q

what other conditions are associated with hypospadias

A

inguinal hernia, and crytorchidism

332
Q

epispadias

A

abnoraml opening of the penile urethra on dorsal surface of the penis due to faulty genital tubercle

333
Q

what are the other conditions associated with epispadias

A

extrophy of the bladder

334
Q

what do the letters of APGAR stand for

A 
A-appearance
P- pulse
G-grimace
A-Activity
R-respiration
335
Q

what is the APGAR score that requires further evalulation

A

7 or under

336
Q

testicular atrophy, long extremities, gynecomastia, female hair distribution, and intellectual disabiltiy- what in the condition and what are the hormonal level with it

A

Klinefelter 47 XXY, it is increased LH and Increased FSH and decreased T and since there is dysgenesis of the seminiferous tubules that is why the FSH is high and the bas normal leydig cells decrease the T and increase the LH and estrogen from the extra androgens hanging around

337
Q

female with short stature, ovary dysgenesis, shield chest webbed neck, cystic hydra, llynpahedam of hands and feet- what in the condition and what are the hormonal level with it

A

it is a Turner syndrome 45XO- there is decreased estrogeen which leads to increased LH and FSH. Some are mosaic which is somatic mosaicism. it is the most common form of primary ammenorhea

338
Q

what are the conditions associated with Turner syndrom

A

bicuspid aortic valve, horseshoe kidney, and coarction of the aorta

339
Q

is pregnancy possible with Turner

A

yes if you give them IVF, exogenous estradiol 17b and progesterone

340
Q

what are double Y males like

A

phenotypically normal but very tall may be assocaited wit severe acne, learning disability, autism spectrum

341
Q

ovotesticular disorder of sexual development

A

both ovarian and testicualr tissue is present wit ambiguous genitalia- true hermaphroditism

342
Q

PCOS- hormones and what happesn

A

hyperinsulinemia and or insulin resistance hypothesized to alter the hypothalamic hormonal feedback response and so this increases LH and FSH and increased androgens like testosterone from the theca cells and this decreases the rate of follicular maturation and leads to unruptured follicles and involution

343
Q

what is the presentation of PCOS

A

it is bilateral large cystic ovaries wit amenorrhea, oligomenrrhea, hirsutism, acnes, and decreased fertility associated with obesitiy

344
Q

what cancer is associated with PCOS

A

endometrial cancer from the opposed estrogen of anovulatory cycels

345
Q

how do you treat PCOS

A

OCPS, weight reduction, clomiphene, ketoconazole, spirolactone

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