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Pathophysiology > Midterm > Flashcards

Midterm Flashcards

1
Q

Sensitivity

A

SNOUT
The ability of a test to be positive in the presence of disease
(TP/TP+FN)
Increased sensitivity means less false negatives
RULES OUT disease if the test in negative

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2
Q

Specificity

A

SPIN
rules in if positive
TN/TN+FP
Specificity increases, and false positive decreases

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3
Q

Epidemiology

A

Discipline that studies the broad behavior of disease in large populations

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4
Q

Incidence

A

Number of new cases of a particular disease that appear in a year

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5
Q

Prevalence

A

Number of people with a certain disease at a given moment

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6
Q

Mortality

A

Number of people dying from a particular disease in a particular period of time

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7
Q

Morbidity

A

Number of people with an illness or complication of an illness and can be stated as either incidence or prevalence

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8
Q

False positive

A

Test is negative but the patient does not have the disease

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9
Q

False negative

A

BAD
Sick patient with normal test result

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10
Q

A negative result in a highly sensitive test

A

High predictive value

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11
Q

A positive result in a highly specific test

A

High predictive test

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12
Q

Labile cells

A

Short life
Abundant stem cells
High continuous retreat I’ve activity
Bone marrow
Epidermis
GI
Bronchial epithelium

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13
Q

Stable cells

A

Long life, abundant stem cells, high regenerative activity with injury
Liver and kidney

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14
Q

Permanent cells

A

No regeneration, scarring only
Brain, heart muscle, skeletal muscle

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15
Q

Cell injury

A

Anoxia, hypoxia, ischemia,
Physical, chemical, radiation, toxins, microbes, inflammation, immune reactions, nutrition, genetic/ metabolic, aging

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16
Q

types of reversible cell change (caused by mild injury or stress)

A

Atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia

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17
Q

Severe cell injury

A

Apoptosis and necrosis

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18
Q

Atrophy

A

Cells shrink

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19
Q

Hypertrophy

A

Cells grow in size
Think skeletal muscle

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20
Q

Hyperplasia

A

Increase in # of cells
Think menses

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21
Q

Metaplasia

A

Change from one cell type to another
Think how smoking changes bronchial epithelium from columnar to squamous, reversible with smoking cessation

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22
Q

Dysplasia

A

Disordered growth
Refers to premalignant changes of cells, usually occurs in epithelium as the uniform appearance and orderly arrangement of cells is replaced by haphazardly arranged, enlarged, and distorted cells with large dark nuclei that reflex chromosomal chaos within
Not invasive, and usually reversible
Think cervical changes

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23
Q

Necrosis

A

PATHOLOGICAL death of cells due to injury
Usually due to vascular ischemia hypoxia/anoxia in a continguous block of cells
4 types- coagulation, liquefactive, caseous, fat necrosis

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24
Q

Apoptosis

A

Natural cell suicide
Carefully regulated, orderly, process

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25
Q

Leukocytes

A

WBCs
Granulocytes, lymphocytes, monocytes

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26
Q

Granulocytes

A

BEN EATS GRANOLA
Basophils
Eosinophils
Neutrophils
Relatively small, multilobed nucleous and a large amt of cytoplasm which contains large granules that are actually lysosomes filled with digestive enzymes
Can crawl through tissues-> diapedesis
And swallow microbes-> phagocytosis
Main cells in acute inflammation and allergic reactions
Constitute 70% of circulating WBCs

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27
Q

Neutrophils

A

Main inflammatory cells in acute inflammation
Main task is phagocytosis
Chemical messenger molecules that communicate to nearby cells or distant organs
67% of WBCs

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28
Q

Eosinophils

A

Less than 3% of WBCs
Principal inflammatory cells in parasitic infections
Also attracted to allergic reactions

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29
Q

Basophils

A

Less than 1% of WBCs
Their blue purple granules contain histamine, responsible for local signs of allergic reactions: swelling, itching, vascular congestion, and mucus production
Similar features as the mast cell
During allergic reactions, they attract other inflammatory cells, including large numbers of eosinophils

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30
Q

Lymphocytes

A

Make up 25% of WBCs
B and T cells
Main cells of the immune system for chronic inflammation

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31
Q

Monocytes

A

5% of circulating WBCs
Macrophages
Large cells with large nucleus and modest amt of cytoplasm with small granules
Monocytes are made in the bone marrow migrate into tissues and then mature into macrophages
Phagocytic

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32
Q

Platelets

A

Fragments of cytoplasm of megakaryocytes- bone marrow cell
Important in blood clotting and inflammation

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33
Q

Autocrines

A

Chemical mediator
Signals that act back on the generating cell
Cell signaling TO ITSELF

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34
Q

Pancrine

A

Molecules are released by nearby cells that act on nearby cells

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35
Q

Hormones (endocrines)

A

Molecules released into the blood stream to act on distant cells

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36
Q

Acute inflammation

A

Follows brief injury, and lasts a few hours to days
Usually from microbial infection- especially bacterial, physical or chemical injury, some immune reactions such as skin rash or poison Ivey

Characterized by vascular dilation, accumulation of edema and inflammation of neutrophils and usually resolves without scarring

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37
Q

Phases of acute inflammation

A

1) before injury
2) immediate vasoconstriction followed by vasodilation
3) vascular wall becomes leaky and endothelial cells become sticky (WBCs adhere to sticky walls)
4) neutrophils migrate through the gaps between endothelial cells
5) Exudate accumulates

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38
Q

Cardinal signs of inflammation

A

Heat
Redness
Swelling
Pain
Loss of function

Also, usually lasts 72 hrs

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39
Q

Chronic inflammation

A

Occurs with persistent injury, usually not severe enough to cause necrosis

  • persistent infection
  • autoimmune disease
  • persistent exposure to injurious agents

An abundance of lymphocytes and macrophages. Few or no neutrophils, attempted regeneration of destroyed cells, scarring, and a rich supply of blood vessels

A mixture of ongoing inflammation and healing

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40
Q

Granulomatous inflammaton

A

Special kind of chronic inflammation
Sheets of macrophages aggregate around a central group of necrotic cells or an infectious microorganism to form tiny inflammatory nodules called granulomas
Features mulinucleated giant cells

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41
Q

CRP

A

C-reactive protien
Made by the liver
Reliable marker of inflammation

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42
Q

First or primary intention

A

Narrow wounds with closely approximated edges
Usually heal in less than a week, leave a smaller scar

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43
Q

Second or secondary intention

A

Deep skin burns or large intestinal ulcers
Broad wounds with widely separated margins

Take several weeks to heal, leave a larger scar

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44
Q

Coagulation necrosis

A

Gel like change in blocks of freshly dead cells
Most common type and occurs in infarcts

Coagulative, to convert fluid into soldi mass

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45
Q

Liquefactive

A

Dead tissue dissolved into fluid
Dead cells are situated or dissolved

Bacterial infection
“Pus” or abscess

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46
Q

Caseous necrosis

A

Variant of coagulative necrosis with limited liquefaction and obliterated cellular detail
The most common cause is TB infection

Cheesy

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47
Q

Fat necrosis

A

Specialized form of liquefactive necrosis that occurs only in fat especially common around the pancreas

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48
Q

Keloid

A

Hyperplastic scar that is prominent, raised, or modular
Not neoplasticism, and rarely anything more than a cosmetic problem

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49
Q

Progenitor granuloma

A

Highly vascular collection of persistent granulation tissue

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50
Q

Innate immunity

A

Present from birth and consists of cellular and molecular defense capabilities that have evolved ability to attack any non-self nonself substance
Response is quick and broad. The inflammatory response is an important element of innate immunity

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51
Q

Adaptive immunity

A

Slower, more programmable system that interacts with invading non self material

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52
Q

Antigen

A

Any substance capable of inciting an adaptive immune response, almost all antigens are non-self proteins though few other large nonself molecules are capable of stimulating an adaptive immune response

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53
Q

Haptens

A

Molecule that illicit an immune response when coupled with a carrier protein

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54
Q

Primary immune response

A

The initial reaction to an antigen, adaptive immunity takes about a week because the immune system has not encountered the antigen in question

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55
Q

Secondary immune response

A

Much quicker, subsequent exposures

(Vaccinations)

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56
Q

Macrophages

A

Phagocytic cells derived from blood monocytes
Circulate freely in the blood into all the tissues, where they roam widely and acquire a colossal appetite for ingesting and destroying microbes and other nonself antigens
Microglia=brain
Kupffer=liver

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57
Q

Dendritic cells

A

Second variety of tissue macrophage, which can evolve from monocytes or lymphocytes
They remain fixed in place
Concentrated in lymphoid organs in tissue exposed to the environment- skin, lunging of respiratory tract, and lining of the GI tract

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58
Q

Antigen presenting cells

A

Dendritic cells and macrophages
Capture antigens and prepare them for representation to t lymphocytes

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59
Q

IgG

A

The smallest and most abundant immunoglobulin in blood, main duty is to neutralize microorganisms. Produced rather slowly and persists a very long time. It confers permanent immunity against reinfection

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60
Q

IgA

A

The most abundant, especially in the GI tract and respiratory membranes, which are open to the environment and exposed to many microorganisms. It also is present in high concentration in tears and in the milk of nursing mothers- which temporarily gives the baby mothers immunity

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61
Q

IgM

A

Is the largest immunoglobulin, hence its alternative name, macroglobulin. It attacks microorganisms and is produced rapidly, providing initial protection while IgG production is getting underway, after which levels fall markedly

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62
Q

IgD

A

Does not appear in blood. It is bound exclusively to the cell membranes of B cells and participates in the process of activating B cells to recognize antigen and undergo clinal expansion

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63
Q

IgE

A

Appears in blood in only trace amounts. The bulk of it attaches to mast cells, the tissue version of basophils. It is important in allergic reactions such as hay fever or skin allergies

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64
Q

Cellular immunity

A

Or delayed immunity
T cell immunity

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65
Q

Humoral immunity

A

B cell system

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66
Q

Cytotoxic T cells

A

Effector cells of cellular adaptive immunity. They target and destroy cells that the immune system identified as containing alien antigen, wither a ca cell or cell affected by virus

CD8, interact with type I MHC

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67
Q

Helper T cells

A

Facilitate the immune activity’s of B cells and other T cells.
CD4+
These cells interact with type II MHC display

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68
Q

Regulatory or suppressor T cells

A

Modulate the immune response to shut down the immune response after successful defense to maintain immune homeostasis and prevent development of autoimmune disease

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69
Q

Memory T cells

A

Enable the cellular immune system to mount a rapid secondary immune response

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70
Q

MHC I

A

Glycoproteins display antigens synthesized in size virus infected or cancerous cell
“This cell is like me, don’t kill me” or “alien antigen present inside; kill me”

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71
Q

MHC II

A

Complexes which are present on the surfaces of macrophages and dendritic cells, whose job is to capture and display external nonself antigen. Like holding up a wanted poster “dangerous invader looks like this, go find it and kill it”

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72
Q

Antigen

A

Is any substance capable of inciting an adaptive immune response, almost all antigens are proteins. The term antigen is usually used in stream of protein when discussing immunity

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73
Q

Type I hypersensitivity
Immediate hypersensitivity

A

Reaction that occurs within a few minutes after an antigen combines with performed antibody created by B cells from an earlier exposure
The earlier episode is called a sensitizing exposure which igE antibodies are secreted by B cells attach to mast cells
The initial episode produces no symptoms, but sets the stage for a rapid reaction on subsequent exposure
-b cell mediated- IgE
-most allergic disorders
-systemic reactions include shock, suffocation, or death

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74
Q

Type II hypersensitivity
Cytotoxic

A

Caused by b cell production of antibodies that react with antigens on the furnace membrane of cells or with extra cellular tissue components
Normal self antigens become seen as nonself by the immune system and become targets for immune attack
Mediated by IgG and IgM that form antigen antibody complexes on the cell surface
- B cell mediated
-Myasthenia Travis
-blood transfusion reactions, hemolytic anemia

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75
Q

Type III hypersensitivity
Immune complex hypersensitivity

A

An immune reaction of B cells in which free/soluble antigen and antibody combine to form an immune complex that deposits in tissue, damaging it and inciting an inflammatory reaction

  • b cell mediated
  • uses compliment system
  • can be systemic hypersensitivity
  • mediated by immune complexes
  • autoimmune pneumonia is (farmers lung)
  • serum sickness, necrotizing vasculitis, glomerulonephritis, RA and SLE
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76
Q

Type IV hypersensitive

A

Cellular (delayed) hypersensitivity
Different from the other types because it is a T cell reaction
No antibodies are produced and the clinical reaction is delayed a few days after antigen contact
-TB
-contact dermatitis- poison ivy, latex gloves, and metallic jewelry
-DM, RA, MS, crohns disease
-transplant rejection

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77
Q

Hypersensitivity mnemonic

A

ACID
Allergic
Cytotoix
Immune complex deposition
Delayed (cell mediated)

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78
Q

Type A can receive…

A

A, O

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79
Q

Type B can receive…

A

Type B and O

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80
Q

Type AB can receive

A

A, B, AB, O
Universal recipient

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81
Q

Type o can receive

A

Type O

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82
Q

RH positive can receive…

A

RH + or -

83
Q

RH negative can receive…

A

RH - only!

84
Q

Active immunity

A

Production of antibodies by ones own immune system such as B cell immunity (endogenous)

85
Q

Passive immunity

A

Antibodies transferred passively to confer temporary immunity as in the case of antibody injections to prevent infection

86
Q

Prions

A

Molecules corrupted form of normal brain protein. Very small
They have no dna or metabolism, they reproduce only by producing more corrupted proteins, much as snowflake
Mad cow disease

87
Q

Endotoxin

A

A component of the cell membrane released as the bacterial organism dies
Can cause a form of vascular collapse called endotoxic shock

88
Q

Exotoxin

A

A product synthesized and excreted by the bacterium (exotoxin)

Living bacteria secretes into the medium which they grow- I.e food powering

89
Q

Two main GPC

A

Staphylococci and streptococci

90
Q

clostridium

A

gram positive anaerobic bacilli
c difficil
c perfirimins
c tetani
c botulinism

91
Q

listeria monocytogenes

A

gram positive bacillus that grows at refrigerator temperature and causes food borne infections through contaminated products
causes bacteremia, meningitis, encephalitis, and dermatitis
pregnant women and the elderly are especially vulnerable

92
Q

Neisseria

A

gram negative cocci
causes meningitis
vaccination
headache, nausea, vomiting, malaise, rash, multple organ failure, shock, dic

93
Q

pseudomonas aeruginosa

A

GNR
opportunistic pathogen frequency causes hospital acquired infections

94
Q

bordetella pertussis

A

GN, short bacillus that is the agent of pertussis or whooping cough, highly communicable disease of children featuring paroxysms of severe coughing accompanies by a final inspiratory whistle- the whoop

95
Q

mycobacterium tuberculosis

A

“acid fast”
tuberculosis(TB)
occurs commonly in the lungs and usually features a period of latency, sometimes for many years following initial infection
-cheesy caseous necrosis
-lesions of secondary TB are characterized by granulomatous inflammation

96
Q

ghon tubercle

A

initial lung lesion in TB, may be associated with similar lesions in infected mediastinal (hilar) lymph nodes- a combination known as ghon complex

97
Q

primary progressive TB

A

usually occurs in children, immunodeficient and elderly. occurs as extensive pulmonary tb which sometimes is associated with widespread blood borne spread to other organs.
pathological appearance is known as milary tb because the various organs contain lots of tiny whitish lesions that look like millet seeds

98
Q

secondary TB

A

reactivation tb, accounts for about 95% of clinical TB
caseating granulomas
arises in previously infected and sensitized person in whom the initial infection was contained by the immune system
A. reactivation TB, arises from dormant primary TB
B. patient has developed a chronic, debilitating disease such as diabetes, chronic lung disease, or malignancy
4. The lesions of secondary TB are characterized by granulomatous inflammation

99
Q

primary TB

A

A. the initial infection of TB
B. ghon tubercle- the initial lung lesion, may also be associated with similar lesions in infected mediastinal lymph nodes ( the combination of these two is ghon compelx)

100
Q

primary infection s.s TB

A

usually asymptomatic except in 5% of patients whom are immunocompromised

101
Q

s/s secondary TB

A

weight loss, fatigue, low grade fever, poor appetite

cough begins to produce sputum, which may be bloody

102
Q

mantoux test, purified protein derivative PPD test

A

skin test for infection of both latent and active cases of TB- not diagnostic of active disease

only the induration is measured, not the erythemia
type IV hypersenitivity

103
Q

gonorrhea
neisseria gonorrhoeae

A

infected mothers can infect the fetus as it passes thought the vaginal canal
s/s
urethritis, proctitis, pharyngitis
females-usually symptomatic but can lead to PID and infertility

104
Q

Trichomoniasis

A

ameba like organism present normally in the vagina of about 10% healthy women. new infection in either sex are usually asymptomatic.
s.s.- females- vaginitis, males- urethritis, balancitis
tx special antimicrobials

105
Q

chlamydiae
chlamydia trachomatis

A

behaves much the same as gonorrhea
women can be asymptomatic carriers

106
Q

syphilis
treponema pallidum

A

untreated develops in four stages: primary, secondary, latent, and tertiary
the hallmark lesion of primary syphilis is the chancer, a hard moist painless ulcer

107
Q

HPV

A

lesions: condyloma acuminatum and squamous carcinoma
vaccination=prevention

108
Q

Rhinoviruses

A

family of over 100 varieties that are the cause of about half of all cases of the common cold.
mode of transmission is usually person to person, droplet possible but less important

109
Q

adenovirus

A

infects the upper respiratory tract causing tonsillitis, similar to strep throat, discussed below, often presents in combination with conjunctivitis
may also cause sever respiratory infections, including croup, bronchiolitis, pna, eat infections or gastroenteritis

110
Q

influenza

A

spread thru respiratory droplets or less often by direct contact
type types, a and b
type a is generally worse

111
Q

rsv
respiratory syncytial virus

A

major cause of lower respiratory tract infections during infancy and childhood
the most common cause of bronchiolitis and pna in children under one year of age

112
Q

rotovirus

A

the most common cause of severe diarrhea among infants and young children

113
Q

norovirus

A

causes 90% of nonbacterial outbreaks of epidemic gastroenteritis around the world
older children and adults are most often affected
transmitted by fecally contaminated food or water by person to person contact and aerosolization
24-4 hours of nausea, abd pain, vomiting, watery diarrhea

114
Q

hydrostatic pressure

A

pushes fluid
the pressure caused by the weight of the fluid

115
Q

oncotic pressure

A

pulls fluid
a measure of the tendency of water to move by osmosis from an area of high water (low solute) concentration across a semipermeable membrane to an area of low water concentration (high solute)

116
Q

hydrodynamic pressure

A

increment of pressure created by resistance to the flow of fluid in a closed system like plumbing pipes or the cardiovascular system
i.e blood pressure

117
Q

exudate

A

inflammatory edema with high protein content
created by vascular permeability of inflammation, which allows protein to leak through capillary walls
does not pit

118
Q

transudate

A

low protein edema
caused by pressure imbalance
either increased capillary fluid pressure or decreased plasma osmotic pressure can cause accumulation of transudate if the net movement of water exceeds lymphatic drainage
PITTING EDEMA

119
Q

RASS system

A
120
Q

aldosterone

A

leads to sodium and water reabsorption back into the circulation and potassium and hydrogen secretion to be lost in the urine

121
Q

angiotensin II

A

converted from angiotensin I by ACE (acetylcholinesterase- an enzyme made in the lungs) which increases blood pressure by:

  • increasing both peripheral resistance and cardiac output
  • simulates the secretion of aldosterone from the adrenal cortex (a steroid that acts upon the kidney to retain sodium and water, which expands blood volume and therefore cardiac output)
  • pituitary gland increases AHD secretion= water absorption
122
Q

Clot

A

begins when plasma or platelets contact something they should not: extravascular tissue or foreign surface
extravascular, platelet plug, fills hole, stops bleeding
forms quickly
normal physiologic mechanism for hemostasis
1)injury
2)temporary vasoconstriction occurs
3) blood contact coagulation cascade activated; platelets accumulate
4) platelet plug forms, fibrin polymerizes from fibrinogen
55) clot forms, bleeding stops

123
Q

extrinsic coagulation pathway

A

initiated when coagulation factor VII comes into contact with tissue factor in the extravascular tissue
takes about 30 seconds to occur

PT

124
Q

intrinsic coagulation pathway

A

pathway is initiated when coagulation factor XII comes into contact with a foreign substance such as glass or plastic
happening inside of the blood
takes about 4-6 minutes to occur

PTT

125
Q

vitamin k

A

must be used to produce factors II, VII, IX, X

126
Q

thrombus

A

collection of cellular elements of blood (plts, wbcs, rbcs) that form only under certain pathologic conditions
◦ requires
‣ endothelial injury
‣ abnormal local blood flow (stasis or turbulence)
‣ hypercoagulability

127
Q

• immune thrombocytopenic purpura (ITP)

A

◦ immune system destroys its own platelets
◦ platlets become coated in antiplatelet antibodies and are quickly removed by the spleen
◦ buisability, epitaxis, bleeding gums, or unusual bleeding after minor trauama
◦ tx-> steroids, splenectomy curative

128
Q

• Thrombotic microangiopathies

A

◦ thrombotic thrombocytopenic purpura (TTP)
‣ likely to occur in adults with neurologic symptoms, renal failure is less likely
◦ Hemolytic uremic syndrome
◦ more likely to occur in children who have renal failure and few neurologic symptoms
‣ HUS strongly associated with gastroenteritis caused by certain strains of e coli

129
Q

• von willebrand disease

A

◦ deficiency of von willebrand factor, a coagulation factor made by endothelial cells and megakaryocytes
◦ lack of vWF interferes with platelet adhesion to the endothelium
◦ inherited disorder

130
Q

• hemophilia (A or factor VIII deficiency)

A

◦ inherited (usually from mothers, unaffected carriers, X linked gene defect)
◦ occurs almost exclusively in males
◦ normal plt and bleeding time
◦ partial thromboplastin time is prolonged because factor VIII is in the intrinsic pathway
◦ periodic tranfusion with factor VIII

131
Q

• Christmas disease (hemophilia B, factor IX deficiency)

A

◦ clinically similar to classic hemophilia but much less common
◦ caused by X factor linked recessive gene defect and it has test abnormalities similar to hemophilia (factor VIII deficiency)

132
Q

Classify hemorrhages by size, and discuss their cause and manifestations.

A

• petechia
◦ smallest hemorrhages about 1mm visible in skin or mucous membranes
◦ buccal or conjunctival mucosal petechiae are usually associated with platelet disorders
◦ thrombocytopenia
• purpura is hemorrhage <1cm
• ecchymosis hemorrhage >1cm
• hematoma is a large collection of blood
• capillary bleeding is most often resulting from a low platelet count
◦ presents as skin/mucosal petechiae, nosebleed, and urinary bleeding

133
Q

disorders with thrombosis risk

A

factor V leiden
SLE

134
Q

• hypovolemic shock

A

◦ underfilled vascular space
◦ hemorrhage
◦ fluid loss
◦ vasodilation
‣ anaphylaxis
◦ acute paralyzing spinal cord injury (neurogenic shock)

135
Q

• cardiogenic shock

A

◦ pump failure
◦ MI, myocardial disease
◦ cardiac muscle lacks the mechanical power to maintain blood pressure

136
Q

• obstructive shock

A

◦ mechanical interference with cardiac output
◦ cardiac tamponade
‣ blood accumulation in the pericardium which prevents cardiac filling

137
Q

• septic shock

A

◦ associated with systemic microbial infection
◦ high morality
◦ toxic molecules from microbes
◦ inflammatory mediators
◦ damaged endothelium-> DIC hemorrhage

138
Q

• 3 stages of shock

A

◦ nonprogessive stage
‣ reflex actions to reestablish perfusion
‣ tachycardia-> increases cardiac output
‣ systemic vasoconstriction (mainly in skin and extremities)
◦ progressive stage
‣ characterized by more severe hypo perfusion and metabolic imbalances
‣ anaerobic metabolism producing lactic acid excess (lactic acidosis)-> vasodilation and pooling of blood in extremities
• depriving brain and abdominal viscera
◦ irreversible stage
‣ progressive severe hypotension, hypoperfusion, and acidosis
‣ decreased myocardial contractility
‣ leakage of blood inflammatory mediators from dying cells
‣ multiorgan failure->death

139
Q

Hypernatremia

A

na+ >145
intracellular dehydration, convulsions, pulmonary edema, hypotension, tachycardia
- fever, flushed skin, restlessness/ irritability), increased fluid retention and increased BP, edema, decreased urine output, dry mouth

dehydrations, pure water deficits, increased renal free water clearance
(weakness, thirst, agitation)

140
Q

hyponatremia

A

serium sodium <135
sodium deficits cause plasma hyposmolality and cellular swelling
-pure sodium loss
-dilutional hyponatremia
- SIADH

s/s lethargy, confusion, decreased reflexes, sz, muscle twitches, ha and coma
neuromuscular irritability
(decreased blood pressure, muscle cramps, headaches, seizers)

141
Q

hypochloremia

A

cl follows na+
usually the result of hyponatremia or elevated bicarbonate ion
develops as the reuslt of vomiting or loss of hcl

142
Q

potassium

A

hydrogen ions accumulate in the ECF during states of acidosis, k+ shifts out of the cell to maintain a balance of cations across the membrane

143
Q

hypokalemia

A

membrane hyperpolarization causes a decrease in neurmuscular excitability
skeletal muscle weakness
smooth muscle atony
cardiac dysrhythmias
-alkalosis, shallow respirations, irritability, confusion drowsiness, weakness, arrhythmias, lethargy, thready pulse, intestinal motility decrease, nausea/ vomiting/ ilius
(arrhythmias, fatigue, weakness, and paresthesias-numbness and tingleing)

144
Q

hyperkalemia

A

slow heart rate, weakness, paralysis, and sensory paresthesias
increased neuromuscular irritability
flaccid paralysis, bradycardia in severe cases
increased resting membrane potential with increased excitability of cardiac muscle

145
Q

trousseaus sign

A

positive and hypocalcemia
Trousseau’s sign refers to the involuntary contraction of the muscles in the hand and wrist (i.e., carpopedal spasm) that occurs after the compression of the upper arm with a blood pressure cuff.

146
Q

chvosteks sign

A

The Chvostek sign is a clinical finding associated with hypocalcemia, or low levels of calcium in the blood. This clinical sign refers to a twitch of the facial muscles that occurs when gently tapping an individual’s cheek, in front of the ear.

147
Q

hypocalcemia

A

muscle fasciculations or tetany, increased reflexes, paresthesias, abdominal cramps, heart arrhythmias
trousseaus and chvosteks sign

148
Q

hypercalcemia

A

◦ hypercalcemia
‣ most common cause is slight hyperparathyroidsm which increases blood pth
‣ malignancy, metastatic to bone, may dissolve bone releasing large volumes of calcium into blood
‣ Fatigue, lethargy, depression, kidney stones, arrhythmias, bone fractures = hypercalcemia

149
Q

ca+ and phosphate

A

have an inverse relationship
increases in Ca, decrease phosphate

150
Q

hypophosphatemia

A

malabsorption syndromes
increased renal excretion of phosphate is associated with hyperparathyroidism
severe cases- irritability, confusion, numbness, coma, convulsions, possibly respiratory failure, cardiomyopathies, bone resorption

151
Q

hyperphosphatemia

A

same as hypocalemia,
kidney failure
-symptoms related to low serum calcium levels

152
Q

hypomagnesemia

A

(lethargy, tremor, tetany, arrhythmias, and sz. )
behavioral changes, irritability, increased reflexes, muscle cramps, ataxia, nystagmus, tetany, convulsions, tachycardia, hypotenison, tetany - increased excitability

153
Q

hypermagnesemia

A

hypotension, depressed respirations, arrhythmias, or cardiac arrest
loss of DTR, skeletal smooth msucle contraction, nausea and vomiting, muscle weakness, hypotension, bradycardia, respiratory distress

154
Q

MCV

A

mean cell volume
average size of an rbc

155
Q

MCH

A

the average amount of hemoglobin int he average RBC

156
Q

MCHC

A

mean cell hemoglobin concentration
the average concentration of hemoglobin per unit of volume in an average RBC is the mean cell hemoglobin concentration

157
Q

macrocytic

A

large RBC

158
Q

microcytic

A

small RBC

159
Q

sickle cell anemia

A

RBCs sickle, and become inflexible, sticky which form plugs in arterioles and capillaries
crisis =presence of trigger (hypoxia, dehydration, infection ect.)

160
Q

acute chest syndrome

A

vaso-occlusive crisis that occurs in the pulmonary vasculature of sickle cell disease
new inflitration on CXR + cough, wheezing, CP, tachynpea, or fever

161
Q

aplastic crisis

A

characterized by an acute drop in hemoglobin level and a markedly reduced number of reticulocytes in the blood
-caused by infection
-rapid drop in hgb
management is with blood transfusion

162
Q

thalassemia

A

microcytic, hypochromic, hemolytic anemia
group of inherited microcytic hmolytic diseases that tend to occur most comonly in people of mediterranean and southeast asian orgin
most severe form is beta thalassemia major (homozygus)
-lack of function hemoglobin
-rbcs do not develop normally
-shortage of mature RBCs
-microcytic anemia develops

163
Q

warm antibodies

A

IgG
most active at normal body temperature
symptoms of warm antibody hemolysis tend to be due to anemia, mild splenomegaly is common

164
Q

cold antibodies

A

IgM
most active at lower temperatures and are precipitated by exposure to cold. symptoms of hemolysis are usually sudden and may be severe: back or leg pain, fever, vomiting/ diahrea, and passage of dark brown urine (hemoglobinuria)

165
Q

iron deficiency anemia

A

microcytic and hypochromic red cells, smaller than nucleous of a lymphocyte

decreased serum Fe, transferrin saturations, increased TIBC, decreased serum Ferritin

decreased Hb, MCV, increased RDW

166
Q

ferritin

A

an iron protein complex found in the bone marrow, liver, spleen, and skeletal muscle

167
Q

transferrin

A

iron is transported from one place to another bound to a special protein called transferrin
measured by testing the ability of transferrin to bind to iron and is expressed as total iron binding capacity (TIBC)

168
Q

megaloblastic anemia

A 
big rbcs!
result from b23 or folic acid deficiency
inturuption of intrinsic factor required for b12 absorption
pernicious anemia (caused by absence of intrinsic factor)
169
Q

RDW

A

redblood cell distribution width
variations in sizes of RBCs

(tend to be high is iron deficiency anemia)

170
Q

left shift

A

left shift: an increased number of band neutrophils is referred to clinically as left shift

  1. band neutrophil- the least mature wbc found in the blood, banana shaped nucleus
  2. “shift towards immaturity”

leukmoid reqaction

171
Q

leukemoid reaction

A

relatively high WBC count over >50,000

in conjunction with a left shift of “band neutrophils” immature

172
Q

lymphocytosis

A

an increase number of lymphocytes in the blood, usually due to viral infection

173
Q

Myeloid malignancies (granulocytes, rbcs, megakaryocytes)

A

acute myeloid leukemia (AML)

174
Q

myeloproliferative syndromes or related myeloid malignanices

A

• chronic myeloproliferative syndromes
◦ chronic myeloid leukemia- malignant granulocytes predominate
◦ polycythemia vera (PV) rare condition but the most common of the myeloproliferative disorders
‣ malignant transformation of the red cell progenitor cells caused by a specific mutation
‣ increased RBC counts, wbc/ plt counts are often high as well
◦ malignant thrombocythemia
‣ essential thrombocythemia is a rare myeloproliferative syndrome that occurs when malignant progenitor cells develop towards megakaryocytes
• plt count is high, dx is one of exclusion of leukemia, polycythemia, and myelofibrosis
◦ primary myelofibrosis
‣ nonmalignant obliteration of normal bone marrow by fiberous tissue (myelophthesis)

175
Q

lymphoid malignancies

(T, B, and NK cells)

A

• ALL, acute lymphoid lymphoblastic leukemia
◦ malignant proliferation of immature lymphocyte precurors, suually b cells, and is the mot common malignancy of children
◦ accumulation of immature blasts in bone marrow that crowd out normal hematopoisesis
• CLL chronic lympoid lymphocytic leukemia and SLL small-cell lympjhocytic lymphoma
◦ different expressons of teh same disease and are often reffered to as CLL/SLL
‣ number of lymphocytes in blood
• few in SLL
• many in CLL
◦ CLL
‣ malignant proliferation of mature b cells that accounts for the about on third of all leukemias, therefore the most common leukemia in the western world
‣ onset slow, most patients are asymptomatic

176
Q

hodgekin lymphoma

A

‣ distinctive microscopic appearence, tends to arise in a single lymph node and spreads slowly in a steo like fashion to adjacent nodes, and is curable in most instances
‣ usually presents as cerbical lymphadenopathy
‣ defective cell-mediated t cell immunity and associated infections
‣ reed-sternberg cell- malignant cell of HL
‣ nodular sclerosing hodkin lymohoma- varient that counts for 70% of cases

177
Q

non-hodgekin lymphomas

A

‣ about 80% of NHL are malignant tumors of b lymphocytes
‣ can arise in not only lymph nodes but other organs such as brain, bone, or bowel
‣ follicular lymphoma- follicular microscopic appearance
• less aggressive
‣ diffuse lymphoma
• grow in uniform microscopic pattern without follicles
• occur mainly in people over 60 years old, but there are two notable age exceptions: childhood and lymphomas associated with aids

178
Q

plasma cell proliferations

A

malignant neoplasm of plasma cells that features multiple bone lesions
‣ solitary myeloma may precede multiple myeloma for many years

179
Q

A. HDL high density lipoproteins

A

a. half protein and half lipid
b. “helpful” cholesterol
c. associated with lower risk of vascular disease

180
Q

B. LDL low density lipoprotein

A

about 22% protein, most of their lipid is cholesterol

a. “lousy” cholesterol, promotes vascular disease
b. high LDL causes atherosclerosis

desirable <100

181
Q

C. very low density lipoproteins (VLDL)

A

about 10% protein, most of their lipid is triglycerides with smaller amts of phospholipid and cholesterol

182
Q

total cholesterol

A

HDL+LDL+VLDl

desirable <200

183
Q

atherosclerosis

A

lifestyle disease associated with unhealthful diet, obesity, smoking, lack of exercise. characterized by fatty deposits in the arterial wall.

the basic lesion is an atheroma

184
Q

primary HTN

A

95% of htn, unknown cuase, no underlying disease can be blamed.

genetics, kidneys (RASS), high na+ intake, obesity/activity level/stress/ smoking

185
Q

secondary HTN

A

5% due to underlying disease

  • renal disease (renal artery stenosis/athrosclerosis-increased renin)
  • steroid hormon excess (cushings)
186
Q

hyaline arteriolosclerosis

A

narrowing of arteriolar lumen and waxy (hyline) degnerative changes in the arteriolar wall

187
Q

hyperplastic arteriosclerosis

A

occurs in severe htn, onion like hyperplasia in the arteriolar wall

188
Q

formation of an atheroma

A
  • endothelial injury
  • lipid accumulation
  • influx of smooth muscle cells and macrophages
  • young atheroma
  • old atheroma- there for good
189
Q

aneurysm

A

dilation of an artery or heart chamber due to the weakness of the wall

-associated with htn and late sphilis

190
Q

vascular dissection

A

E. vascular dissection- longitudinal tearing within the wall of an artery, most often the aorta caused by blood that enters the wall through a defect in the lining- usually a tear or ulceration in an atheroma

-usually predisposed by HTN or marfan/ehlers-danlos syndrome

191
Q

◦ temporal arteritis

A

chronic granulomatous inflammation of large and medium sized arteries

HAs, scalp tenderness, visual or neuroloigcal problems, paoin in jaw muscles during chewing, fever

192
Q

takaysu arteritis

A

◦ takaysu arteritis characterized by granulomatous inflammation in the aorta and its main branches

193
Q

◦ thromboangiitis obliterans (buerger disease)

A

affects small and medium size vessels in the hands and feet. common in young heavy cigarette smokers

194
Q

◦ polyarteritis nodosa

A

autoimmune diseases of small and medium size muscular arteries- tend to affect kidneys and abdominal viscera

195
Q

◦ kawasaki disease

A

‣ important cause of acquired heart disease in children because of its predilection to affect coronary arteries
‣ also known as mucocutaneous lymph node syndrome, fevers conjunctivitis oral ulcers, redness of palps and soles, rash, lymphadenopathy

196
Q

◦ microscopic polyangiitis

A

hypersensitivity vasculitis

197
Q

wegener granulomatosis

A

vasculitis affected small to medium size arteries in the nose, throat, sinuses, lungs, and kidneys of middle-aged men

198
Q

hemangiomas

A

benign, small, red-blood filled lesions composed of capillary size blood vessels

199
Q

kaposi sarcoma

A

malignant tumor often found in aids patients caused by HHV8

200
Q

pyogenic granuloma

A

small nodular collection of inflamed capillaries usually found on the skin

e.i the healing umbilical stump of a newborn or in the oral cavity

201
Q

lymphangiomas

A

collections of lymphatic capillaries, less common than hemangioma

usually benign and found in subcutaneous tissues of head and neck

202
Q

angiosarcoma

A

rare malignant tumor of vascular endothelial cells that occurs most frequently in the skin, breast tissue, soft tissue, and liver

203
Q

cardiac biomarkers

A

troponin rises within 4-6 hours, peaks 10-24 hrs, detected for up to 10-14 days

CK, CK-MB is cardiac specific, rises within 3-6hours, peaks at 12-24 hours, returns to baseline within 12-48 hours

Pathophysiology (4 decks)

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