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Blue Flags Flashcards

1
Q

incidence

A

number of new cases/number of people at risk

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2
Q

prevalence

A

number of existing cases/total number of people in pulation

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3
Q

what does short disease duration do to incidence and prevalence

A

they should be roughly equal

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4
Q

what does long disease duration do to incidence and prevalence

A

prevalence increases over incidence because of the increased number of cases

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5
Q

type 1 error

A

false positive

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6
Q

type 2 error

A

false negative. related to the statistical power

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7
Q

t test

A

checks the difference between 2 means

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8
Q

ANOVA

A

checks the differences between the means of 3 or more groups

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9
Q

Chi-square

A

checks differences between 2 or more percentages or proportions or categorical outcomes

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10
Q

informed consent

A

disclosure of pertinent information, ability to comprehend the information, capacity o make own decisions, voluntary freedom from coercion, understand proposed treatment, outcomes, alternative options, risks and benefits

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11
Q

patient is non adherent

A

determine reason for non adherence and determine the willingness to change

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12
Q

desire unessecary procedure

A

understand why they want the procedure and address underlying concern, Do not reduce or refer to another

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13
Q

patient struggles to take medication

A

provide written instructions, attempt to simplify regiments, use teach back method

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14
Q

family members ask for information about prognosis

A

avoid discussing issues with relatives without the patients permission

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15
Q

family member asks physician to not disclose the results of the test if the prog is poor because the patient will not handle it well

A

attempt to identify why they think this information will be harmful to the patient. Explain that the patient has decision making capacity until there is communication otherwise

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16
Q

17 year old girl requests an abortion

A

require parental consent.

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17
Q

parents want girl to give up child of 15 yo pre girl

A

girl has rights about the child. discuss options if requested

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18
Q

terminally ill patent requests physician assisted suicide

A

refuse involvement of the physician but can prescribe medically appropriate analgesics that coincidentally shorten the patients life

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19
Q

patient is suicidal

A

assess the seriousness of the threat suggest the patient remain in the hospital and if not make them stay

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20
Q

patient thinks you’re attractive

A

ask direct, close ended questions and use a chaperone. NEVER DATE

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21
Q

a woman who had a mastectomy says she now feels ugly

A

find out why the patient feels this way

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22
Q

patient is angry about wait time

A

acknowledge the anger and do not take it personally. Do not explain the delay

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23
Q

patient is upset with how they were treated by another doctor

A

suggest that the patent speak directly to that physician directly about the concerns

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24
Q

an invasive test is performed on the wrong patient

A

inform the patient of the mistake

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25
Q

requires a treatment not covered by insarance

A

never delay or limit care based on this. Discuss all options even if they are not covered

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26
Q

a boy loses his sister and now feels responsible

A

5-7 year olds understand death is permanent and all life function is gone. Proved a direct concrete description of his sisters death. Normalize fear and feelings and encourage lay and healthy coping behavior

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27
Q

common causes of death by age- under 1

A

congenital malformations, Preterm birth, SIDS

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28
Q

common causes of death- 1-14 years

A

unintentional injury, cancer, congenital malformation

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29
Q

common cause of death 15-34 years

A

unintentional injury, suicide, homicide

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30
Q

common cause of death 35-44

A

unintentional injury, cancer, heart disease

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31
Q

common cause of death 45-64

A

cancer, heart disease, unintentional injury

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32
Q

common cause of death 65+

A

heart disease, cancer, COPD

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33
Q

hospital conditions with high readmission rate- medicare

A

congesitive HF, septic, pneumonia

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34
Q

hospital conditions with high readmission rate- medicaid

A

mood disorder, schizophrenia, DM

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35
Q

hospital conditions with high readmission rate- private insurance

A

chemo radiation, mood disorder, complications of surgery

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36
Q

hospital conditions with high readmission rate- uninsured

A

mood disorder, alcohol related, DM

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37
Q

delirium symptoms

A

waxing and waning level of consciousness with acute onset, rapid decrease in attention span and arousal. Disorganized thinking, hallucinations, altered sleep, cognitive dysfunction- slowing EEG

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38
Q

delirium causes

A

CNS disease, UTI, trauma, substance abuse, withdrawal, metabolic or electrolyte disturbance, hemorrhage, urinary or fecal retention. can be medication related in the elderly especially anticholinergics

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39
Q

delirium treatment+ what not to give

A

use haloperidol and treat underlying condition. Do not give benzos because this can worsen it in the elderly unless its for alcohol withdrawal

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40
Q

dementia

A

decreased intellectual function without affecting consciousness. Characteristic memory deficits, apraxia, aphasia, agnosia, loss of abstract thought, behavioral/personality changes, impaired judgement. Can develop delirium.

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41
Q

dementia causes- irreversible

A

AD, Lewy body dementia, HD, Pick, cerebral intact, Mad cow, chronic substance abuse

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42
Q

reversible causes of dementia

A

hypothyroid, dpression ,B12 def, NPH, neurosyphillus, hydrocephalus

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43
Q

EEG in delirium vs. dementia

A

Delirium has a diffuse slowing EEG and dementia has a normal EEG

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44
Q

major depression how long before diagnossi

A

need 2 weeks for symptoms

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45
Q

major depression treatment

A

CBT and SSRI

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46
Q

major depression symptoms

A

depressed mood, sleep disturbance, loss of interest, guilt or feelings of worthlessness, energy loss and fatigue, concentration problems, appetite/weight changes, psychomotor retardation or agitiation, suicidal ideations

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47
Q

depression sleep changes

A

decreased REM latency, decreased slow wave sleep, increased REM early in the cycle, increased REM overall, repeated nighttime awakening, early morning awakening

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48
Q

dysthymia

A

persistent depressive disorder- mild depression lasting at least two years

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49
Q

atypical depression

A

mood reactivity- able to cheer up, reversed vegetative, hypersomnia, hyperphageia, leaden paralysis, interpersonal rejection sensitivity

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50
Q

Cluster A

A

paranoid, schizoid, schizotypal

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51
Q

pervasive distrust and suscpiciousness; projection is the major defense mechanism

A

paranoid

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52
Q

voluntary withdrawal from social situations, limited emotional expression, content with social isolation

A

schizoid

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53
Q

eccentric appearance, odd beliefs, or magical thinking, awkward in relationships

A

schizotypal

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54
Q

Cluster B

A

antisocial, borderline, histrionic, narcissitic

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55
Q

cluster C

A

avoidant, OCPD, dependent

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56
Q

disregard for and violation of rights or others, criminality, M>F, goes by another name before the age of 18

A

antisocial

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57
Q

unstable mood and interpersonal relationships, impulsive, self-mutiliation, suicidal, sense of emptiness, splitting

A

borderline

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58
Q

excessive emotionality and excitability, attention seeking, sexually provocative, overly concerned with appearance

A

histrionic

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59
Q

grandiose, sense of entitlement, lacks empathy and requires excessive admiration, often demands the best and reacts with rage to criticism

A

narcissistic

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60
Q

hypersensitive to rejection, socially inhibited, timid, feelings of inadequacy, desires relationships with others

A

avoidant

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61
Q

preoccupation with order, perfectionism and control. behavior bothers others but not self

A

OCPD

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62
Q

submissive, clingy, excessive need to be taken care of, exceedingly low self-confidence

A

dependent

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63
Q

Fab region

A

fragment antigen binding- determines the unique antigen binding pocket only 1 antigen per B cell

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64
Q

Fc region

A

constant region, carboxy terminus, complement binding, carbohydrate side chains

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65
Q

Generation of antibody diversity

A

random recombination of VJ and D genes which are for the chains. The random addition of nucleotides to a DNA during recombination by terminal TDT determine this and then there is a random assignment of light chains to heavy chains

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66
Q

generation of antibody specificity

A

somatic hypermutation and affinity matuation- variable switching, isotype switching

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67
Q

what can antibodies do

A

prevent bacterial adherence (neutralization), opsonixation (promotion of phagocytosis), complement activation activates C3B and the mac complex

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68
Q

what antibody is the most abundant in the serum

A

IgG

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69
Q

what antibody fixes complement, crosses placenta, opsonizes bacteria, and neutralizes bacterial toxins and viruses

A

IgG

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70
Q

what antibody prevent attachment of bacteria and viruses to mucus membrane

A

IgA

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71
Q

what antibody is produced by the GI tract and protects against gut infecttions

A

IgA

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72
Q

what antibody is released into the secretions like tears, saliva, mucus and breast milk

A

IgA

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73
Q

what antibody is the first response to an antigen

A

IgM

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74
Q

what antibody fixes complement but does not cross the placenta

A

IgM

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75
Q

Pentamer antibody

A

IgM

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76
Q

what antibody is found on the surface of B cells

A

IgD

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77
Q

what antibody binds mast cells and basohils

A

IgE

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78
Q

what antibody cross links when exposed to allergen mediating the type I HSN through release of histamine

A

IgE

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79
Q

what antibody mediates defense against worms

A

IgE

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80
Q

recurrent bacterial and enteroviral infections like giardia and increased encapsulated infections. There are no B cells in the peripheral blood and decreased Ig of all classes. No tonsils or lymph nodes

A

defect in BTK which leads to no B cell maturation and X linked recessive called Bruton agammaglobulinemia

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81
Q

Airway and Gi infections with atopy, and autoimmune and anaphylaxis to blood products. Decreased IgA and normal others. Celiac is common. Recurrent sinus infections

A

selective IgA deficiency- must wash red blood cells

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82
Q

20-30 yo patient with increased autoimmune diseases, bronchiectasis, lymphoma, sinopulmonary infections. decreased plasma cells and decreased immunoglobulins

A

defect in B cell differntiation- Common variable immunodeficiency

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83
Q

Tetany, hypocalcemia, recurrent viral and fungal infections, conotruncal abnormalities like tetralogy of Fallot and truncus arteriosis. Decreased T cell and PTH, decreased Ca. absent thymic shadow,

A

Thymic aplasia like Digeorge. It is from 3 and 4 pharnygeal pouch failure

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84
Q

disseminated mycobacterial and fungal infections may present after administration of BCG (Tb vaccine), decreased IFN gamma, decreased Th1 response

A

IL12 deficiency

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85
Q

coarse facies, cold staph abscesses, retained primary teeth, increased IgE, dermatologic problems. decreased interferon gamma

A

deficiency of Th17 cells so impaired recruitment of neutrophils to sites of infections- autosomal dominant hyper IgE syndrome

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86
Q

noninvasive candida infections of the skin and mucous membranes. Absent invert T cell proliferation response

A

T cell dysfunction- chronic mucocutaneous candidiasis

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87
Q

failure to thrive, diarrhea, thrush, recurrent infections like PJP. treated with Bone marrow transplant. Decreased T cell receptor excision circles, absence of thymus shadow, no germinal centers, and no T cells.

A

SCID- defective IL2R gamma chain. Adenosine deaminsase deficiency

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88
Q

cerebellar defects, spider angiomas, IgA deficiency- increased AFP, decreased IGA, IGG, IGE. lymphopenia and cerebellar atrophy

A

defect in ATM gene- failure to repair DNA double strand breaks- arrest the cell cycle- Ataxia telangactasia

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89
Q

severe pyogenic infections early in life with opportunistic infections like PJP, cryptosporidium, and CMV. Normal IgM but decreased IgG, A, and E

A

defective CD40L on Th cells that impaired class switching- hyper IgM

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90
Q

Thrombocytopenia, eczema, recurrent infections, increased autoimmune disease- increased IgE and IGA but decreased G and M

A

WAS mutation so T cells are unable to reorganize actin cytoskeleton- Wiskott Aldrich

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91
Q

Recurrent bacterial skin and mucosal infections, absent pus formation, impaired wound healing, and delayed cord separation. increased neutrophils not in the infection site

A

Defect in LFa1 so impaired migration and chemotaxis and is autosomal recessive- Leukocyte adhesion deficiency

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92
Q

recurrent staph, strep, and albinish, peripheral neuropathy, progressive neurodegeneration, infiltrative lymphocytosis, griant granules in the granulocytes and platelets. pancytopenia, mild coagulation defects

A

Chediak Higashi Syndome

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93
Q

increased catalase positive infections- nocardia, pseudomonas, listeria, aspergillum, candida, icily, staph, serration, b coppice, h pylori- nitroblue is not reduces

A

chronic granulomatous disease from NADPH oxidase deficiency

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94
Q

deficiency leads to chalices with inflammation of lips scaling and fissures of the corners of the mouth and corneal vascularization-

A

B2 riboflavin

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95
Q

what does B2 do

A

component for redox reactions

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96
Q

deficiency of this leads to glossitis, severe leads to pellagra, with diarrhea, dementia, and dermatitis with broad collar rash with hyper pigmentation of the skin

A

niacin deficiency

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97
Q

what is Hartnup disease

A

AR recessive deficiency ot tryptophan and so there is aminoacidura and decreased gut absorption and this means decreased niacin

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98
Q

excess of this leads to facial flushing, hyperglycemia and hyperuriciemia

A

this is niacin

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99
Q

what can niacin trat

A

lower levels of VLDL and raises levels of HDL because its part of NAD and NADP

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100
Q

deficiency causes dermatitis, enteritis, alopecia, and adrenal insufficiency

A

this is from B5 or pantothenic acid

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101
Q

deficiency leads to convulstiona, hyper irritability, peripheral neuprpathy, sideroblasts dur to impaired hemoglobin- and causes

A

B6 deficiency- isoniazid and oral contraceptives

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102
Q

function of B6

A

used for NT

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103
Q

deficiency causes dermaittis, alopeica, enteritis- eats lots of egg whites

A

biotin of B7- ued for putuvate carboxylase, acetyl coz to alony coa, oropionyl coa and methylamolnyl coa

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104
Q

deficiency leads to macrocytic megalibalstic anemia, hyperhsegmented polymophonuclear cells, glossitis, no neurology symptoms. increased homocysteine. see in what two risk groups

A

folic acid or B9- seen in pregnancy and alcoholics

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105
Q

deficiency of microcytic and megaloblastic anemia, hypersegmented PMN< prothesis, subacute combined degeneration, corticospinal tracts, and abnormal myelin. increased homoystein and methylmalonic acid. Prolonged deficiency leads to nerve damage- what can cause it

A

stored in the liver and taken up in the terminal ileum, malabortiptio from sprue or enteritis, liver fluke, pernicious anemia, gastric bypass crowns or vegans

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106
Q

deficiency swollen gums, brusing, petichaie, hemarthorosis, anemai, poor wound healing, perifollicular and subperiosteal hemorrhages with corkscrew hairs

A

cannot hydroxylate proline and lysine for collagen synthesis- vitamin C

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107
Q

excess is vomiting, nausea, fatigue, calcium oxalate nephrolithiasis, and increased risk of iron toxicity

A

vitamin C

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108
Q

deficiency- rickets ostomalacia, and tetany from the hypocalcemia

A

D- breastfed do not get it oral low sun exposure, pigmented skin

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109
Q

what enzyme activates vitamin D

A

alpha 1 hydroxylase

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110
Q

excess ledas to hypercalcemia, hypercalciuria, loss of appetite, stupor, and grnaulomas

A

vitamin D

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111
Q

def- hemolytic anemia, acanthocytosis, muscle weakness,posterior collumn and spinocerebellar tract demyelination- no megaloblastic aneia or increased methylamlonic acid- looks the same as B12 def

A

vitamin E

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112
Q

what does vitamin E do

A

it is an antioxidnat

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113
Q

def leads to neonatal hemorrhage with increased PT and PTT but normal bleeding time. neonatal have sterile Gi so cannot make it yet or prolonged antibiotics

A

vitamin K

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114
Q

what does fetus look like with K def

A

intracranial pressure and refused vaccin

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115
Q

deficiency leadsto delayed wound healing, hypogonadism, decreased axillary hair, dysgeusia, anosmia, acrodermatitis enteropathica- why and what

A

zinc can be from small intestine malabsortion

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116
Q

protein malnutrition resulting in skin lesions, and edema from decreased plasma oncotic pressure.

A

Kwashiorkor

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117
Q

total calorie malnutrition resulting in emaciattion like tissue and muscle wasting and loss of subcutaneous fat

A

marasmus

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118
Q

rate limiting enzyme for glycolysis

A

phosphofructokinase 1

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119
Q

rate limiting enzyme for gluconeogenesis

A

Fructors 1 6 bisphosphate

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120
Q

rate limiting enzyme for TCA

A

isocitrate dehydrogenase

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121
Q

rate limiting enzyme for glycogenesis

A

glycogen synthase

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122
Q

rate limiting enzyme for glycogenolysis

A

glycogen phosphorylase

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123
Q

rate limiting enzyme for HMG shunt

A

G6PD

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124
Q

rate limiting enzyme for de novo pyrimidine synthesis

A

CPS2

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125
Q

rate limiting enzyme for de novo purine synthesis

A

PRPP amidotransferase

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126
Q

rate limiting enzyme for urea cycle

A

CPS1

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127
Q

rate limiting enzyme for fatty acid synthesis

A

acetyl coa carboxylase

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128
Q

rate limiting enzyme for fatty acid oxidation

A

carnithine acyltransferase I

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129
Q

rate limiting enzyme for ketogenesis

A

HMG CoA synthase

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130
Q

rate limiting enzyme for cholesterol synthesis

A

HMG reductase

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131
Q

when is hexokinase used and what are its enzymatic properties

A

it is in most cells and it has a low km but high affinity but low Vmax

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132
Q

when is glucokinase used and what are its enzymatic properties

A

only in the liver and on Beta cells of the pancreas. It is insulin dependent. Need a lot of glucose to use it, but it has a high km but high Vmax so very efficient

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133
Q

derivatives of phenylalanine

A

tyrosine, thyroxine, dopa, melanine, dopamine, NE, epi

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134
Q

derivatives of tryptophan

A

niacin, serotonin, melatonin

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135
Q

derivatives of histidine

A

histamine

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136
Q

derivatives of glycine

A

porphyrin, heme

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137
Q

derivatives of glutamate

A

GABA and glutathione

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138
Q

derivatives of arginine

A

creatine, urea, nitric oxide

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139
Q

severe fasting hypoglycemia, increased glycogen in the liver, increased blood lactate, increased triglycerides and increased uric acid and hepatomegaly- what is the deficiency, enzyme, and treatment

A

Von Gierke disease- glucose 6 phosphatase deficiency- treat with frequent glucose and corn starch and avoid galactose and fructase- impaired gluconeo and glycogenolysis

140
Q

patient has cardiomegaly, hypertrophic cardiomyopathy, exercise intolerance and some systemic symptoms-what is the deficiency, enzyme, and treatment

A

lysosomal alpha 1,4 glucosidase with alpha 1,6 activity- defiency- Pompe trashes the pump- heart, liver, and muscle

141
Q

patient has normal blood lactate but accumulate of limit dextrin in the cytosol- some hypoglycemia-what is the deficiency, enzyme, and treatment

A

defieincy in the deb ranching enzyme- alpha 1,6 glucosidase- gluconeogenesis is intact will see branch end points

142
Q

paient has increased glycogen in the muscle, but the muscle cannot use it. they have painful muscle cramps, red urine with strenuous exercise, and arrthymia from electrolyte issues- have some second wind from increased muscle blood flow-what is the deficiency, enzyme, and treatment

A

deficient in glycogen phosophorylase and myophosphorylase- McArdle- blood glucose is unaffected

143
Q

episodic peripheral neuropathy, angiokeratomas, hypohidrosis, and progressive renal failure and heart disease later in life-what is the deficiency, enzyme, and treatment, and what accumulates

A

Fabry disease-deficient in alpha galactosidase A and accumulate ceramide trihexosidase- it is the only one that is x linked recessive

144
Q

hepatosplenomegaly, pancytopenia, osteoporosis, aseptic necrosis of the femur, bone crisis, lipid laden macrophages with tissue paper-what is the deficiency, enzyme, and treatment, and what accumulates

A

Glucocerbrosidase- beta glucosidase- build up of glucocerebroside- Gaucher

145
Q

progressive neurodegeneration with hypotonia, hepatosplenomegaly, foam cells, and cherry red macula-what is the deficiency, enzyme, and treatment, and what accumulates

A

sphingomyelinase deficiency with sphingomyelin increased- Nieman Pick

146
Q

progressive neurodegeneration, developmental delay, cherry red macula, onion skin lysosomes, no hepatosplenomegaly-what is the deficiency, enzyme, and treatment, and what accumulates

A

hexosaminidase A build uo of GM2 ganglioside

147
Q

peripheral neuropathy, developmental delay, optic atrophy, globoid cells and seizures-what is the deficiency, enzyme, and treatment, and what accumulates

A

Krabbe- galactocerebrosidase

148
Q

central and peripheral demyelination with ataxia and dementia–what is the deficiency, enzyme, and treatment, and what accumulates

A

Metachromic leukodystrophy- arylsulfatase A

149
Q

developmental delay, coarse face and joints, airway obstruction, corneal clouding, and hepatosplenomegaly–what is the deficiency, enzyme, and treatment, and what accumulates and inheritance

A

Hurler- alpha L iduronidase- heparin and dermatin sulfate build up- AR

150
Q

aggressive behavior, no corneal clouding, coarse face and joint pain-what is the deficiency, enzyme, and treatment, and what accumulates and inheritance

A

Hunter- iduronate sulfatase- heparin and dermatin sulfate- XR

151
Q

weakness hypotonia and hypoketotic hypoglycemia-what is the deficiency, enzyme, and treatment, and what accumulates

A

carnithine deficiency- inherited defect in transport of LCFA into the mitochondria leading to toxic accumulation

152
Q

patient has vomiting, lethargy, seizures, coma, liver dysfunction with hypoketotic hypoglycemia–what is the deficiency, enzyme, and treatment, and what accumulates

A

avoid fasting- decreased ability to break down fatty acids- medium chain acyl cos dehydrogenase deficiency

153
Q

what leads to an increased risk of UTI

A

vesicoureteral reflux

154
Q

what is there determining risk factor for UTI from cathertization

A

the duration of catheterization

155
Q

what is the leading cause of UTI

A

ecoli

156
Q

what is the second leading cause of UTI in sexually active women

A

staph spare which is novobiocin resistant

157
Q

what is the cause of UTI that has large mucoid capsule and colonies that are viscous

A

klebsiella

158
Q

what are UTI that have red pigment and drug resistant

A

serratia

159
Q

UTI with swarming motility and produces urease

A

proteus

160
Q

UTI with blue green pigment and fruity odor- long term indwelling catheter

A

pseudomonas

161
Q

no inflammation, but thin white vaginal discharge with dish ordor and clue cells

A

gardenerlla- treat with metronidazole

162
Q

strawberry cervix, forthy yellow green, foul smelling discharge, motile

A

trichomonas- metronidazole

163
Q

inflammation with thick white cottage cheese, with pseudohyphae

A

candida and use azoles

164
Q

congenital infection: bug, and transmission- chorioretinitis, hydrocephalus, and intracranial calcifications and blueberry rash

A

cat feces, toxoplsmosis

165
Q

congenital infection: bug, and transmission, and mom- abnormalities of the eye, including catarachts, deafness, PDA, and blueberry mffin rash

A

respiratory droplets, maternal has arthralgia, lymphadenopathy- rubella,

166
Q

congenital infection: bug, and transmission, and mom- blueberry rash, hearing loss, seizures, poetical rash, and periventricular calcifications

A

sexual contact or organ transplant, mono illness in mom- CMV

167
Q

congenital infection: bug, and transmission, and mom- recurrent infections, chronic diarrhea

A

sexual contact or needlestick, low CD4 count, and HIV

168
Q

congenital infection: bug, and transmission, and mom- encephalitis and vesicular lesions

A

skin mucus membranes, asymptomatic in the mom or some ulcerated lesions HSV 2

169
Q

congenital infection: bug, and transmission, and mom- hydrops detalis, facial notched teeth, and saddle nose, saber shins, deafness

A

syphilis- from sex- chancre or disseminated in stage 2

170
Q

STI lesion- painful genital ulcer with exudate and inguinal adenopathy

A

chancroid- haemophilus ducreyi

171
Q

STI lesion- urethritis, cervicitis, epiddimitis, conjunctivitis, reactive arthritis, PID

A

chylamydia D-K

172
Q

STI lesion- warts and koilocytes

A

condylopma accumoinata- HPV

173
Q

STI lesion- painful penile, vulvar, and vercival lesions, ulcers, systemic symptoms such as fever headache, myalgia

A

HSV2

174
Q

STI lesion- urethritis, PID, prostatitis, epidydimitis, arthritis, creamy purulent discharge

A

gonorrhea

175
Q

STI lesion- jaundice

A

HBV

176
Q

STI lesion- infection of lymphatics, painless genital ulcers, painful lymphadenopathy, buboes

A

lymphogranuloma venereum- C trachomatis L1-L3

177
Q

STI lesion- painless chancre

A

trponema pallidum- primary syphillus

178
Q

STI lesion- fever, lymphadenopathy, skin rashes, condyloma lata

A

secondary syphilis

179
Q

STI lesion- gummas, tabes dorsalis, general paresis, aortitis, argyll robertson pupil

A

tertiary syphilis

180
Q

STI lesion- vaginitis, strawberry cervis, motile on wet prep

A

trichomonas

181
Q

cervical motion tenderness, purulent discharge, salpingitis, hydrosalpinx, and tubo-ovarian abscess

A

PID

182
Q

what can happen from PID

A

ectopic pregnancy, pelvic pain, adhesions

183
Q

what is Fitzhugh Curtis Syndrome

A

infection of liver capsule and violin string adhesions of peritoneum to liver

184
Q

what is the Michaelis Menten- what is K, an what is Vmax

A

Km is inversely related to the affinity of the substrate, so the lower the Km the tighter the binding. The Vmax is directly proportional to to the enzyme concentration. The max is when it is saturated.

185
Q

what changes with Michaelis-Menten if there is a competitive inhibitor

A

It means that the vmax stars the same, but the Kmax is higher,

186
Q

what changes with Michaelis-Menten if there is a non competitive inhibitor

A

The vmax decreases

187
Q

In regards to the Lineweaver Burke plot- what is the y axis and x axis

A

yaxis is 1/V and x axis is 1/concentration of substrate

188
Q

In regards to Michaelis-Menten- what is the y axis and x axis

A

y axis is V and x axis is concentration of substrate

189
Q

In regards to the Lineweaver Burke plot- what happens if the V max decreases

A

The y intercept is increased as max decreases

190
Q

if there is a reversible competitive inhibitor, what is the effect of Vmax and Km

A

vmax is unchanged and Km increases

191
Q

If there is a irreversible competitive inhibitor, then there is

A

a decrease in Vmax and KM is unchanged

192
Q

if there is a noncompetitive inhibitor then there is

A

a decrease in Vmax and Km is unchanged

193
Q

Which inhibitor can be overcome with increased substrate

A

the reversible competitive inhibitor can be overcome with substrate

194
Q

If there are curves then how do you calculate the bioavailability

A

F=(area under curve oral x IV)/(area under IV curve x oral dose)

195
Q

what happens with oral bioavailability- why does it decrease with oral

A

High first pass metabolism through the liver leads to decreased serum drug

196
Q

where is absorption of rectum based on pectinate line

A

if below the pectinate line, it can increase bioavailability because of systemic circulation. If it is above the pectinate line, it can go through portal circulation so there is decreased drug

197
Q

What is bioavailability of IV

A

it is 100%

198
Q

What is the volume of distribution and formula

A

It is the theoretical volume occupies by the total amount of drug in the body relative to plasma concentration. Apparent Vd of plasma portion bound drugs can be altered by the liver and kidney disease, so decreased binding to protein leads to increased Vd. Vd= amount of drug in body/plasma concentration and Vd=drug in IV/ drug in plasma

199
Q

what is the Vd in the blood

A

low Vd because large charged molecules stay bound

200
Q

what is the Vd in the ECF

A

it is medium, and small hydrophobic molecules

201
Q

what is the Vd in all tissues including fat

A

It is high and small lipophilic molecules attached to protein

202
Q

clearance of a drug- definition and formula

A

the volume of plasma cleared of drug per unit time. Clearance may be impaired with defects in cardiac, hepatic, or renal function. Clearance= rate of elimination of drug/plasma concentration of the drug=Vd x Ke or Cl=.7Vd/t.5

203
Q

half life definition and formula

A

the time required to change the amount of drug in the body by 1/2 during elimination. t.5= .693Vd/Cl

204
Q

what is the percent eliminated at 1,2,3,4 half lives

A

1 is 50%, 2 is 75%, 3 is 87.5%, and 4 is 94%

205
Q

what is the equation for loading dose

A

Css x Vd= loading dose

206
Q

what is the equation for maintenance dose

A

MD= Css x Clearance

207
Q

what does renal and liver disease do to maintenance dose

A

it decreases the maintenance dose and doesn’t change the loading dose

208
Q

what is the additive effect of drug interactions

A

effect of substance A and B together is equal to the sum of their individual effects

209
Q

what is the permissive effect of drug interactions

A

presence of substance A is required for the full effects of substance B

210
Q

what is the synergistic effect of drug interactions

A

effect of substance A and B together is greater than the sum of their individual effects

211
Q

what is the tachyphylactic effect of drug interactions

A

acute decrease in response to a drug after initial or repeated administration.

212
Q

with a competitive antagonist, what happens to the potency and efficacy and an example

A

The curve shifts right, so the potency is decreased but there is no change in efficacy because it can be overcome which the addition of substrate- diazepam and flumazenil

213
Q

with a noncompetitive antagonist, what happens to the potency and efficacy and an example

A

It shifts the curve down, so there is decreased efficacy that cannot be overcome with increased substrate. An example would be- NE and pehnoxybenzamine

214
Q

with partial agonist, what happens to potency and efficacy and an example

A

It acts at the same site as full agonist, but with lower maximal effect, so decreased efficacy and potency is independent- morphine and buprenorphine.

215
Q

what increases SV

A

increased contractily, increased preload, and decreased after load. a failing heart has decreased SV

216
Q

what ions increase contractlity

A

increased intracellular Ca and decreased extracellular NA- digitalis exploits this by raising the intracellular NA and Ca but working on the NA Ca exchanger.

217
Q

what do venodilators do to preload

A

decreased preload

218
Q

draw a pressure volume loop and label

A

yay

219
Q

S1 heart sound

A

M and T close

220
Q

S2

A

a p close

221
Q

S3

A

increased with increased filling pressures like mitral regard or heart failure or dilated ventricles

222
Q

S4

A

heart as an atrial kick in late diastole from the atria having to contract more forcefully against the hypertrophied ventricles

223
Q

JVP a wave

A

atrial contraction

224
Q

JVP x wave

A

atrial relaxation

225
Q

JVP c wave

A

RV conration

226
Q

JVP v wave

A

is the RAP increasing from filling

227
Q

JVP y wave

A

the RV is filling from the RA

228
Q

what does handgrip do to murmurs

A

it increases the after load which increases mitral regurg, and aortic regard and creates a later MVP click

229
Q

what does valvalva do to murumurs

A

decreases the preload to it increases hypertrophic cardiomyopathy

230
Q

what does rapid squatting do

A

it increases venous return, preload and after load which increases the intensity of AS and decreases the hypertrophic cardiomyopathy murmur

231
Q

crescendo decrescendo murmur systolic- delayed pulses, syncope, angina, dypnea-

A

AS

232
Q

what is AS usually from

A

calcification of a bicuspid or normal valve

233
Q

holosystolic hugh blowing murmur

A

regurg

234
Q

holosystoic high pitched blowing murmur that radiates towards the axilla- what is it and whats it from

A

MR from ischemic heart disease, MVP, Lv dilation

235
Q

holosystolic high pitched blowing murmur that is in the right sternal border

A

causes by RV dilation- TR

236
Q

late systolic crescendo murmur with mid systolic click. due to sudden tensing of the chordae tendinae- heard over the apex. Loudest just before S2- what and why

A

MVP from myxomatous degeneration from connective tissue disorder, and rhematic fever or chord rupture

237
Q

holosystolic harsh murmur over the right sternal border

A

VSD

238
Q

high pitched blowing murmur in the early diastolic time with head bobbing and wide pp. what and why

A

it is AR from aortic root dilation from bicuspid aortic valve, rhenmatic never, syphillus, marfan, endocarditis, and leads to let HF

239
Q

opening snap in diatole and late rumble what and why

A

MS- the S2 and OS correlate with severity and the LA is greater than LVP- it can be from rheumatic fever and lead to LA dilation

240
Q

continuous machine mumur on S2

A

PDA can be from congenital rubella and closes with indomethacin and prostaglandin E keeps it open

241
Q

what does increased serotonin do to the heart

A

it increases the fibroblasts which leads to increased fibornous tissue leading to tricuspid regard and pulmonary valve isses

242
Q

what can AS go to if it decompensates

A

can go to HF with afib and its because the decrease in CO and loss of contraction meds to decreased ventricular filling and so it decreases the preload and leads to severe hypotension and acute pulmonary edema

243
Q

what are the most commonly occluded coronary vessels

A

LAD>RCA>circumflex

244
Q

what is the change in the myocardium after 0-4 hours

A

no change

245
Q

what is the change in the myocardium after 4-12 hours

A

wavy fibers and long myocytes and nuetrophils begin to appear

246
Q

what is the change in the myocardium after 12-24 hours

A

myocyte hypereosinophilia with pyknotic nuclei

247
Q

what are the issues associated with reperfusion

A

generation of free radicals and leads to hyper contraction of myofibrils through increased Ca influx

248
Q

what are the major complications in the first 24 hours

A

entricular arrythmia, HF, cardiogenic shock

249
Q

what is the change in the myocardium after 1-3 days

A

extensive coagulative necosis, acute inflammation with neutrophils- lose nuclei and striations

250
Q

what are the complications in the 1-3 day post MI period

A

postinfarction fibrinous pericarditis

251
Q

what is the change in the myocardium after 3-7 days

A

disintegration of dead neutrophils and myofibers macrophages at the edges

252
Q

what is the change in the myocardium after7-10 days

A

robust phagocytosis and granulation tissue

253
Q

what is the change in the myocardium after 10-14 days

A

granulation with neovaculature

254
Q

what are the biggest complications between 3-14 days post MI

A

free wall rupture leading to tamponade
papillary muscle rupture- mitral regurg holosytolic murmur
interventricular septal rupture due to macrophage mediated structureal degradation
LV pseudoaneursym- risk of rupture creating a VSD

255
Q

what is the change in the myocardium after 2weeks to months

A

contracted scar

256
Q

what are the complications after 2 weeks to several months

A

dressler syndrome, HF, arryhmias, true ventricular aneurys, with risk of mural thrombis

257
Q

LAD MI elevations in

A

V1-V4

258
Q

RCA MI elevations in

A

II, III, AVF

259
Q

LCX MI elevations in

A

I and AVL

260
Q

what drugs decrease mortality in HF patients

A

beta blocker, spiro, and aCE

261
Q

what is the systolic dysfunction in HF

A

decreased EF and increased EDV, decreased contratility due to ischemia or dilation of the heart

262
Q

what is the diastolic dysfunction in HF

A

decreased compliance, preserved EF< normal EDV but decreased compliance due to hypertrophy

263
Q

what are the symptoms of let heart fialure

A

orthopnea, paroxysmal norcutnal dyspnea, pulmonary edema

264
Q

what are the symptoms of right heart failure

A

hepatomegalty, jugular venous distnetion, peripheral edema

265
Q

Giant cell arteritis- what is the histology of the vessel like

A

intimal thickening, lamina fragmentation and granulomatous nflammation- can read to ophthalmic artery occlusion

266
Q

Takayasu arteritis

A

asian females under 40 with pulses upper extremities, fever, night sweats, arthritis, myalgia, skin nodules, ocular disturbance. Granulomatous thickening and narrowing of the aortic arch

267
Q

what is the determinant of the severity of giant cell arteritis

A

IL6- the drug is toertizumab for this

268
Q

if a person has polyarteritis nodosa what might they also have

A

HBV

269
Q

what are the symptoms and histology of polyartertitsi nodosa

A

fever, weight loss, mailase, headache, abdominal pain, melena, hypertension, neurologic dysfunction, cutanoues eruptions, renal damge- usually is transmural inflammation of the arterial wall with fibrinoid necrosis leading to read lmicroaneurysms. It is also immune complex mediated

270
Q

Kawasaki what is the presentation

A

asian children under 4 conjunctival injection, rash, adneopathy, strawberry tongue, hand and foot changes, fever- fever is for 5 days

271
Q

what is the long term complication of Kawasaki and what is the treatment

A

coronary artery aneursym and aspirin

272
Q

buerger- presentation and histology- thromboangitis obliterans

A

heavy smokers, male with intermittent claudication and gangrene and autoamputation of the digits. get segmental thromosing vasculitis it extends to contiguous vessels and nerves

273
Q

granulomatosis with polyangitis- pathology and what is seen

A

perforation fo nasal septum, chronic sinusitis, otitis media, mastoidis, hemptypsis, cough, dyspnea, hematuria, red cell casts- focal necrotizing vascultitis, necrotizing granulomas in the lung and upper airway, necrotizing glomerulonephritiss

274
Q

microscopic polyangitis

A

ncrotizing vasculitis of the lung, kindy and skin with pouch immune glomerulonepthitis and palpable purport without nasal involvement

275
Q

eosinophilic granulomatosis with polyangitis

A

asthma, sinusitis, skin nodules or purport, peripheral neuropathy, heart, GI ,kidneys, pauci immune glomerulonephritis- granulomatous necrotizing vasculitis with eosinophilia- increased IgE

276
Q

Henoch Schonlein purpura

A

URI then skin with palpable purport on the legs and butt, arthralgia, abdominal pain, vasculitis from IgA complex deposition. HSN III from deposition of complexes in the small vessels

277
Q

where is preproinsulin synthesized

A

rough ER

278
Q

when is c peptide and insulin increased

A

sulfonylureas or diabetic drugs that increase the release of insulin or insulinomas

279
Q

when is insulin and not cpeptide increased

A

it is when there is an exogenous source of insulin- this can be from factitious disorder or malingering

280
Q

what does insulin do to target tissues

A

it brings insulin receptors and it induces glucose uptake into dependent tissues

281
Q

what kind of activity does insulin receptors have

A

tyrosine kinase activity

282
Q

what are the effects of insulin

A

increased glucose transport to skeletal muscle and adipose tissues, increased glycogen synthesis and storage, increased T G synthesis, increased NA retention, increased cellular uptake of K and amino acids, decreased glucagon, decreased lipolysis

283
Q

what glucose receptors are on adipose and skeletal muscle

A

GLUT 4

284
Q

what glucose receptors are insulin dependent

A

GLUT 4

285
Q

what glucose receptors are on RBC, brain, cornea, placenta

A

GLUT 1

286
Q

what glucose receptors are on beta cells, liver, kidney, small intestine

A

GLUT 2

287
Q

what glucose receptors are on spermatocytes and GI tract and take in fructose

A

GLUT 5

288
Q

what glucose receptors are on brain and placenta

A

GLUT 3

289
Q

what is the pathway of insulin release from the beta cell

A

glucose enters the beta cell and it increases ATP which closes the K channels and this depolarizes the membrane allowing for Ca to diffuse across the membrane and this causes the release of insulin by exocytosis

290
Q

why is there an increased response to glucose if it is oral instead of IV

A

there are increased incretins if it is given orally which increases the beta cell sensitivity to glucose. Incretins are also called GLP1

291
Q

what drugs block aromatase

A

anastrozole, exemestane

292
Q

what drug blocks five alpha reductasse

A

finasteride

293
Q

male has ambiguous genitalia and XX has no secondary sexual dev- increased aldosterone, decreased cortisol, decreased sex hormones, increased BP, and decreased K

A

17 alpha hydroxylast deficiency

294
Q

males look normal and have precociuos puberty and females are virilized- decreased aldosterone, decreased cortisol and increased sex hormones, decreased BP, increased BP- increased renin activity, increased 17 hydroxyprogesterone

A

21- hydroxylase

295
Q

females are virilized and males look normal- decreased aldosterone but increased 11 deoxycorticosterone so it increased BP, decreased cortisol, increased sex hormones, increased BP, decreased K and decreased renin activity

A

11 Beta hydroxylase

296
Q

what is the cheat for CAH

A

1 in the first digit is HTN and 1 in second digit is virilized

297
Q

DM type 1 characteristics, genetics, glucose intolerance,

A

autoimmune destruction of beta cells due to glutamic acid decarboxylase antibodies,always insulin for treatment, under 30 years, no obesity, relatively weak genetics, it is HLA DR3 and 4, and insulin sensitivity, ketoacidosis, Bcells are decreased, decreased insulin levels- classic stmpyoms

298
Q

what is the histology of DM 1

A

islet leukocytic infiltrate

299
Q

DM 2 characteristics, genetics, glucose tolerance

A

increased insulin resistance, progressive pancreatic beta cell failure, sometimes need unselling, best, very genetic, mild to moderate glucose intolerance, some amyloid deposition i the pancreas,

300
Q

what is the histology of DM 2

A

islet amyloid polypeptide- IAPP deposits

301
Q

the patient is pregnant for 20 days, what should be formed

A

the neural plate should be formed

302
Q

when does the notochord and neural development take place

A

18-20 days

303
Q

draw circle of willis

A

are you a winner?

304
Q

what is the rule of 4’s

A

4 midline M’s- morot math, medial lemnisucs, MLF, motor CN
4 side S;s- spinocerebella, spinothalamic, sensory V1, sympathetic
4 CN motor are midline and divisible by 12: 3,4,6, 12

305
Q

what cranial nerves are in the midbrain

A

3,4

306
Q

what cranial nerves are in the pons

A

5,6,7,8

307
Q

what cranial nerves are in the medulla

A

9,10,12

308
Q

what crainal nerve is not in the brianstem

A

11

309
Q

contralateral paralysis and sensory loss of the face and upper limb, aphasia if dominant usually the left, and it is the left hemisphere. hemineglect if lesion is nondominat- what vessel is occluded

A

middle cerebral artery

310
Q

contralateral paralysis and sensory loss of lower limb cam have some behavioral and urinary incontience- what vessel is occluded

A

anterior cerebral artery

311
Q

contralateral paralysis and or sensory loss- face and body. absence of cortical signs like neglect, aphasia, visual field loss- what vessel is occluded

A

lenticulostriate artery

312
Q

what does the lenticulostriate artery supply

A

striatum and internal capsule

313
Q

what are the common reasons for lenticulostrate artery lesions

A

lacunar strokes from uncontrolled hypertension

314
Q

contralateral paralysis of lower limbs, decreased contralateral proprioception, and ipsilateral hypoglossal dysfunction tongue deialtion laterally- what vessel is occluded

A

anterior spinal artery

315
Q

medial medullary syndrome

A

infart of paramedic branches of the asa and or vertebral arteries

316
Q

vomitting, vertigo, nystagmus, pain and temperature sensation decreased from the ipsilateral face and contralateral body:dysphagia, hoarseness, decreased gag reflex, ipsilateral kroner syndrome ataxia, dysmetria- what vessel is occluded and what is the syndrome called

A

posterior inferior cerebellar artery- laterally medially syndrome

317
Q

what area is covered by PICA

A

it is vestibular nuclei, lateral spinothalamic tract, spinal trigeminal nucleus, neucelus ambiguus, sympathetic fibers, inferior cerebellar peduncle

318
Q

vomiting vertigo nystagmus, paralysis of the face, decreased lacrimation, salivation, decreased taste, ipsilateral pain and temperature of the face and contra of decreased pain and temperature of the body- ataxia and dysmetria– what vessel is occluded

A

AICA- lateral pons syndrome-facial droop

319
Q

preserved consciousness, vertical eye moevement, blinking, quadriplegia, loss of voluntary mouth, facial and tongue movement– what vessel is occluded

A

basilar artery

320
Q

contralateral hemianopia with macular spearing- contralateral paresthesias, numbness of less and trunk- can’t recognize faces- what vessel is occluded

A

posterior cerebral artery

321
Q

Weber syndrome

A

anterior midbrain infarct from occlusion of the paramedic branches of the posterior cerebral artery- peduncle lesion causes dysphagia, dystonia, dysarthria, contralateral spastic hemiparesis, CN III palsy and eyes are down and out

322
Q

repetitive brief heaches, excrutiating periorbital pain with lacrimation and rhinorrhea, may present with horner syndrome

A

cluster headache

323
Q

what is the treatment for cluster headache

A

it is sumatriptan and O2 and prophylaxis for verapamil

324
Q

bilateral- steady pain so photophobia or phonophobia with no aura

A

tension headache

325
Q

pulsating pain with nausea, photophobia, phonophobia, aura- due to irritation of CN V, meninges, or blood vessels release of substance P, cancinton gene- related peptide vasoactive peptides

A

mirgraine

326
Q

treatment for migraine

A

NSAID, triptans, dihydroergotamine, beta blocks, ccb, amytripyltine,

327
Q

dihydroergotamine

A

induce vasospastic angiana contricts vasuclat smooth muscle and partial agonist for sertonin recptors

328
Q

positional vertigo

A

inner ear etiology with semicircular canal debris, vestibular nerve infection, ,inure disease and positional testing- delayed horizonatal nystagmus

329
Q

what are the symptoms of deniers disease

A

vertigo, tinnitus, hearing loss- increased pressure and volume of endolymph, recurrent vertigo, ear fullness and pain. unilateral sensineural hearing loss and tints.

330
Q

central vertigo

A

brain stem or cerebellar lesion stroke affecting vestibular nuclei or posterior fossa tumor. Directional change of nystagmus, skew deviation, diplopia, dysmetria, positional testing. immediate nystagmus in any direction, focal neurologic

331
Q

Sturg Wber syndrome

A

congenital non-inherited somatic developmentally animal of neural crest derivatives due to GNAQ gene. affects small blood vessels and port wine stain in the V1/V2 birth mark. Ipsilateral leptomeningeal angioma with seizures and epilepsy and intellectual disability and episcelral hemangiona- increased intraocular pressure- early onset flaucoma

332
Q

what is the typical finding of sturg weber

A

tram track calcifications on opposing dyri

333
Q

TS findings

A

hamartomas, angiofibromas, mitral regurgiation, ash lead spots- cardiac rhabdomyosarcoma- rental angiomyolipoma and ungal fibromas

334
Q

NF1

A

cade au last spots, litchi nodules- iris hamartomas, cutaneous neurofibromas, optic gliomas, heochromocytoma, mutated NF1, inactivation of RAS on chromosome 17-derived from neural crest cells

335
Q

VHL

A

hemangiobalstomas- high vascularity with hyper chromic nuclei and in retina and brain stem, cerebellum, spin, angiomatosis (cavernous hemangioma in skin mucosa and organs), bilateral renal cell carcinoma and pheochromocytoma

336
Q

osteoporosis what are the lab values

A

normal lab values

337
Q

osteopetrosis what are the lab values

A

decreased Ca

338
Q

pagets what are the lab values

A

increased ALP

339
Q

osteitis fibrous cystica/primary hyperparathyroid what are the lab values

A

increased CA, decreased phos, increased ALP, increased PTH

340
Q

secondary hyperparathyroid what are the lab values

A

decreased CA, increased phos, increased ALP, increased PTH

341
Q

osteomalacia/rickets what are the lab values

A

decreased CA, decreased phos, increased ALP, increased PTH

342
Q

hypervitamin D what are the lab values

A

increased Ca, increased phos, decreased PTh

343
Q

pink pearly lesions with telanagtasia and rolled borders with central ulcers and palisading nuceli

A

basal cell carcinoma

344
Q

lower lip, hand, ears, local innovation with ulcerative red lesion with frequent scale, adnd chronic draining sinuses has keratin pearls

A

squamous cell carcinoma

345
Q

S100 tumor marker and associated wit sunlight and fair skinned persons. depth correlate with mets, ABCS and superficial and depth is associated wit prognsosi

A

melanoma

346
Q

neprhotic and nephrtitic syndromes

A

FA 548

Step1 (9 decks)

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