Patho Quiz 1

Front 1

TBW=

Back 1

ICF(2/3) + ECF (1/3).
Movement to a fro via osmosis

Front 2

Infants have highest

Back 2

% TBW. Immedate postnatal loses 5%

Front 3

Why do older people have less water?

Back 3

kidneys dont concentrate urine as well. & thirst perception dec

Front 4

What is the responsible ion of ECF fluid?

Back 4

Sodium

Front 5

WHat is the responsible ion of ICF fluid

Back 5

potassium

Front 6

What forces favor filtration?

Back 6

Capillary hydrostatic pressure and interstitial oncotic pressure

Front 7

What forces oppose filtration

Back 7

plasma oncotic pressure & interstitial hydrostatic pressure

Front 8

What does favoring refer to

Back 8

out of the capillary and into the interstitial space

Front 9

What are the four most common mechanisms which produce edema

Back 9

1. Increased hydrostatic pressure
2. Decreased plasma oncotic pressure
3. Increased capillary membrane permeability
4. Lymphatic obstruction

Front 10

Example of inc hydrostatic pressure

Back 10

Venous obstruction, salt and water retention – DVT’s, tight clothing

Front 11

What conditions cause salt and water retention?

Back 11

CHF and kidney failure

Front 12

What causes Decreased plasma oncotic pressure

Back 12

Liver disease, malnourishment (LESS PROTEIN, third spacing), hemorrhage, burns

Front 13

What causes Increased capillary membrane permeability

Back 13

Burns, crushing injuries, neoplasms, allergic reactions

Front 14

What causes lymphatic obstruction

Back 14

Lymphedema, non functional lymphnode or lymph removed.

Front 15

localized edema is limited to

Back 15

area of trauma

Front 16

Generalized edema is

Back 16

dependent, pitting edema

Front 17

Third spacing may lead to a state of

Back 17

dyhydration. severe burns, sequestering- shock

Front 18

What are the clinical signs of edema?

Back 18

pulmonary edema, weight gain, swelling, puffy....coughing SOB & pleural effusion, ascites

Front 19

What do you do for the swelling of edema?

Back 19

Compression socks, diuretics, limit salt intake

Front 20

Isotonic fluids

Back 20

no shrinking or swelling of cells

Front 21

How do you get isotonic depletion?

Back 21

hemorrhage, burns, & dehydration

Front 22

how do you get excess isotonic

Back 22

excess fluid resuccitation, drugs or too much aldosterone?

Front 23

Hypertonic

Back 23

water loss, cells shrink. occurs in hypernatremia and a deficit of water

Front 24

Hypotonic

Back 24

water gain, cells swell, occurs in hyponatremia and an excess of free water

Front 25

loss of water can occur via

Back 25

inc resp rate bc water loss from lungs

Front 26

signs and symptoms of hypernatremia =

Back 26

thirst fever dry mouth, hypotension, tachycardia, low venous pressure & restlessness

Front 27

dehydration is a misnomer for

Back 27

simultaneous water and salt loss

Front 28

True dehydration is a

Back 28

pure water deficit but rearely exists because most people have access to water

Front 29

Sx of dehydration include

Back 29

thirst, dry skin, elevated temp, weightloss and concentrated urine, dec skin turgor, may have sx of hypovolemia

Front 30

how does hyponatremia occur?

Back 30

Sodium loss, not taking in enough sodium or dilution of serum sodium levels

Front 31

What are the signs of hyponatremia?

Back 31

confusion, lethargy, sz

Front 32

What are causes of water excess?

Back 32

water intoxication, ARF, CHF, cirrhossi, renal disease....SIADH

Front 33

what are signs of hypokalemia?

Back 33

neuromuscular and cardiac: leg cramps muscle weakness, prolonged q wave, prominent u wave

Front 34

What are causes of hyperkalemia

Back 34

cell trauma, massive crush inj, long surgery

Front 35

What are the levels of hypocalcemia?

Back 35

serum ca <8.5, ionized level <4.0

Front 36

why does blood administration lead to low ca

Back 36

the citrate soln binds to ca in blood

Front 37

what happens to heart with low CA

Back 37

dec conractility, prolonged QT

Front 38

What is the level of hyper calcium?

Back 38

>12

Front 39

What are causes of high calcium

Back 39

hyper PTH, bone mets, sarcoidosis,

Front 40

What are the levels of phoshate?

Back 40

> 2.0 and < 4.5

Front 41

What problem can cause hypophasphate

Back 41

Shift to left.....cause SZ, confusion....caused by respiratory alk, refeeding, DKA, exc in stool & urine

Front 42

What can cause hyper phosphatemia

Back 42

chemo causes cell death which releases into blood stream

Front 43

what are the levels for mag?

Back 43

1.5-2.5

Front 44

Hypomag mimicks

Back 44

hypocalcemia

Front 45

hemoglobin is a

Back 45

weak acid (buffer)

Front 46

Low pH stimulates

Back 46

lung hyperventilation and kidneys to excrete H as NH4

Front 47

Metabolic alkalosis caused by vomiting depletes

Back 47

ECF and chloride so it is called hypochloremic metabolic alkalosis

Front 48

resp alkalosis sx

Back 48

include headache, restlessness, blurred vision, tremors, convulsions

Front 49

blue bloaters

Back 49

bronchitis

Front 50

Pink puffers

Back 50

emphysema (vasodilation from acidosis)

Front 51

what causes respiratory alkalosis

Back 51

lung disease, CHF, high altitudes, fever, anemia, thyrotoxicosis, cirrhosis, and gram neg sepsis

Front 52

• Invasion

Back 52

alteration in met cell function, cell death
– Resists host defenses; attaches to host cells

Front 53

Multiplication

Back 53

– tissue damage, symptomatic
– Uses host nutrients and environment for
reproduction

Front 54

Spread

Back 54

– Migrates locally or through bloodstream and
Lymphatics *FEVER

Front 55

1st line defense mechanisms

Back 55

skin, mucous membranes, innate immunity

Front 56

2nd and 3rd line defense mech

Back 56

inflammation & adaptive immunity

Front 57

innate immunity =

Back 57

vaccination

Front 58

adaptive immunity =

Back 58

fever, redness

Front 59

what are the microcircuation changes at vascular level

Back 59

inc vasc permeability & vasodilation

Front 60

adaptive immunity is comprised of

Back 60

antigens

Front 61

what are antigens

Back 61

designed oo afford long term protection against particular invading microorganisms. Have memory function immunoglobins, antibodies, lymphocytes....specificity & memory

Front 62

The complement system

Back 62

marks the bacteria for destrucion

Front 63

macrophages

Back 63

enlist other attackers

Front 64

Helper T cells are activates and

Back 64

activate B cells

Front 65

B cells produce antibodies which

Back 65

bind to invaders and are killed by killer T cells

Front 66

What are the 3 forms of antigenic variation to bypass host barriers

Back 66

• Mutation → antigenic drift
• Recombination → antigenic shift
• Gene switching → turning on/off of surface molecules

Front 67

Bacterial need what and may steal it from host

Back 67

iron....steal from transferrin & hgb

Front 68

What pathogens spread too quickly for immune syst

Back 68

rotavirus, hantavirus, strep, group b strep

Front 69

Toxins

Back 69

released from bacteria, cause fever & redness

Front 70

Bacteria that produce endotoxins are called

Back 70

pyrogenic bacteria because they activate the inflammatory process and produce fever

Front 71

endotoxins inc capillary permeability b activating

Back 71

anaphylotoxins. ....so 2 fold inc n cap permeability allows lg volumes of plasma to leave and causes the hypotension we see in sepsis

Front 72

Adsorption

Back 72

virus binds to the host cell.

Front 73

Penetration

Back 73

virus injects its genome into host cell

Front 74

Viral Genome Replication

Back 74

viral genome replicates using the host's cellular machinery.

Front 75

Assembly

Back 75

viral components and enzymes are produced and begin to assemble

Front 76

Maturation

Back 76

- viral components assemble and viruses fully develop.

Front 77

Release

Back 77

newly produced viruses are expelled from the host cell.

Front 78

Superficial
Dermatophytes producing

Back 78

tineas (ringworm, athletes foot...)

Front 79

central thermostat

Back 79

hypothalamus

Front 80

exogenuous pathogens will form

Back 80

outside host....do not produce fever

Front 81

endogenuous pathogens

Back 81

produced with in host, will cause fever

Front 82

pencillin inhibits

Back 82

synthesis of cell walls

Front 83

rifampin

Back 83

alters the metabolism of nucleic acid

Front 84

clindamycin

Back 84

inhibits protein synthesis

Front 85

how does HIV work?

Back 85

suppresses the immune response bc it infects and destroys the helper Tcells. generalized immune deficiency

Front 86

Pyrimidines

Back 86

• Single carbon nitrogen rings
• Cytosine and Thymine

Front 87

– Purines

Back 87

• Double carbon nitrogen rings
• Adenine and Guanine

Front 88

Adenine always pairs with

Back 88

Thymine

Front 89

Guanine always pairs with

Back 89

cytosine

Front 90

genetic code is directed by

Back 90

codons...64 possible group

Front 91

Most important enzyme of replication procedure. Makes sure bases are complementary

Back 91

DNA polymerase. makes corrections if finds mistake

Front 92

types of mutation

Back 92

1. inherited alteration of genetic material
2. base pair substitution
3. frameshift mutation
4. mutagens cause mutations

Front 93

Congential defects are caused by mutations

Back 93

replacing a nucleotide where another should be and the mistake is not caught for whatever reason.

Front 94

If there is a change but no consequence it is called a

Back 94

silent substitution

Front 95

Frameshift mutation

Back 95

insertion or deletion of one or more the base pair molecules

Front 96

helicase

Back 96

unwinds dna

Front 97

What pairs with adenine in RNA

Back 97

uracil

Front 98

How is RNA diff?

Back 98

ribose instead of deoxyribose, U-A, and single stranded

Front 99

WHat does mRNA do?

Back 99

synthesisze RNA from DNA template

Front 100

Exons....

Back 100

stay while introns are removed

Front 101

Where does Transcription happen

Back 101

in nucleus

Front 102

where does translation happen?

Back 102

outside nucleus

Front 103

what binds to the promoter site and unstrands the Dna and exposes unattached DNA bases to be exposed

Back 103

RNA polymerase

Front 104

What is Translation?

Back 104

RNA direction of polypeptide (protein) synthesis

Front 105

What does tRNA do?

Back 105

tells mRNA what to synthesize

Front 106

Translation occurs on the

Back 106

ribosome

Front 107

What does the anticodon do?

Back 107

talks with mRNA to dictate exactly what amino acid sequence should be produced

Front 108

Polypeptide is what

Back 108

protein

Front 109

autosomes=

Back 109

22 pairs of ahromosome

Front 110

homologous pair in

Back 110

females

Front 111

gametes cells are

Back 111

sex cells

Front 112

somatic cell are

Back 112

non sex cell

Front 113

picture of chromosomes called a

Back 113

karotype

Front 114

Triploidy-

Back 114

3 copies of each chromosome=3*23

Front 115

Tetraploidy=

Back 115

92 chromosomes

Front 116

What is accountable for 10% of all miscarriages?

Back 116

Triploidy & tetraploidy

Front 117

Aneuploidy

Back 117

somatic cell that does not contain a multiple of 23 chromosomes

Front 118

Trisomy

Back 118

a cell containing three copies of one chromosome

Front 119

Monosomy

Back 119

a cell containing only one copy of a given chromosome

Front 120

monosomy of any autosome is

Back 120

is lethal and unsurvivable

Front 121

aneuploidy occurs

Back 121

by the process of nondisjunction

Front 122

Trisomy 21=

Back 122

downs syndrome

Front 123

what are common ailments of downs

Back 123

diff fight resp infx, susceptibile to leukemia, AD by 40 years old

Front 124

women <30 have a what chance to have downs baby

Back 124

1/in 1000-1/2000 .
at 45 the risk is 3-5%

Front 125

Trisomy X

Back 125

3 X's. no distinct physical abnormaility....but sterility, menstrual irregulary or mental retardation

Front 126

Turner syndrome

Back 126

Single X, with no homologous X or Y chromosome. Female, sterile, gonadal streaks, short, webbed neck

Front 127

Kleinfelter Syndrome

Back 127

At least 2 X and a Y chromosome. Male, sterile,tall, hippy

Front 128

Cridu chat syndrome.

Back 128

deletion on chromosome 5. low birth weight, severe developmental delay, microcephaly, heart defects and a typical facial appearance.

Front 129

Robertsonian translocation

Back 129

two nonhomologous chromosomes fuse at the centromere and form on large chromosome. Only occur in certain chromosomes that have little genetic material and typically a short arm of the chromosome.. Usually no physical symptoms but have only 45 chromosomes

Front 130

What is RT responsible for?

Back 130

3-5% of downs....affects the person's offspring

Front 131

Fragile X Syndrome

Back 131

2nd most common form of genetic retardation. Duplication of CGG sequence.

Front 132

spot where gene is on chromosome

Back 132

locus

Front 133

genes at a particular locus can take different forms

Back 133

allele

Front 134

compostiion of genes at a given location

Back 134

genotype

Front 135

genotype +environment

Back 135

phenotype

Front 136

Who is the father of genetics?

Back 136

gregor mendel

Front 137

Genomic imprinting is more common in

Back 137

more common in IVF

Front 138

achrondroplasia

Back 138

autosomal dominant , dwarfism

Front 139

Penetrance is

Back 139

percentage of individuals who have a specific genotype who also exhibit the expected phenotype

Front 140

Incomplete penetrance

Back 140

may be that individuals who have the genotype do not exhibit the phenotype at all even if the disease has been transmitted to the next generation.

Front 141

Obligate carriers are those individuals

Back 141

who are known carriers of an autosomal dominant trait because they have an affected parent and affected child but do not have the disease themselves.

Front 142

Huntington’s disease is an example of

Back 142

age dependent penetrance.

Front 143

Genomic imprinting is when

Back 143

when a mutation inherited from the father or the mother give different clinical symptoms.

Front 144

Dosage compensation is

Back 144

that one of the x chromosomes in women are inactive because when x linked diseases are seen they are typically in equal severity on men and women.

Front 145

Sex determination region on the

Back 145

Y (SRY)

Front 146

Incidence rate

Back 146

number of new cases of a disease reported during a specific period divided by the number of individuals in the population

Front 147

Prevalence rate

Back 147

proportion of the population affected by a disease at a specific point in time. Affected by the incidence rate and length of a survival period in affected individuals

Front 148

calc relative risk

Back 148

incidence rate of disease among exposed to risk factor/
incidence rate of the disease among individuals not exposed to risk factor

Front 149

What is the threshold of liability

Back 149

the point on the curve where they go from unaffected to affected

Front 150

Empirical Risk

Back 150

Risks based on direct observation of data

Front 151

multifactoral inheritance

Back 151

risk higher if more than one family member is affected.

Front 152

If a twin pair shares a trait then

Back 152

concordant

Front 153

if twin does not share trait then

Back 153

disconcordant

Front 154

Congential Malformations

Back 154

2% risk, 1‐5% sibling recurrence risk

Front 155

family hx of CAD has

Back 155

2-7x more likely to develop

Front 156

What % of HTN is due to genetics

Back 156

20-40%

Front 157

if first degree relative has Breast cancer

Back 157

2x risk

Front 158

if have the BRCA gene

Back 158

50-80% lifetime risk

Front 159

first degree relative has colon cancer

Back 159

2-3x risk

Front 160

Experience stress when a demand exceeds

Back 160

persons coping ability

Front 161

Alarm stage

Back 161

when a stressor triggers the actions of the hypothalamus and SNS

Front 162

Stage of resistance or adaptation

Back 162

occurs with the actions of the adrenal hormones cortisol, norepinephrine and epinephrine

Front 163

Stage of exhaustion

Back 163

marks continuous stress, unsuccessful adaptation and body impairment

Front 164

reactive response

Back 164

is a physiologic response derived from psychologic stressors

Front 165

Anticipatory response

Back 165

no reaction to a stressor but physiologic response like reacting to a certain predator

Front 166

Conditional response

Back 166

learning that certain things are associated with certain feelings i.e. danger, fear

Front 167

Stress response is initiate by corticotropin releasing hormone....CRH is released from the

Back 167

hypothalamus, SNS, pituitary gland, adrenal gland

Front 168

the SNS arousable causes

Back 168

the medulla of the adrenal gland to release catecholamines (80% ep, 20% norepi)into the blood stream

Front 169

both catecholamines bind to

Back 169

alpha and beta receptors

Front 170

Norepinephrine causes

Back 170

vasoconstriction of smooth muscle and raises blood pressure, dilates pupils of the eye, increases sweat gland action in the armpits and palms

Front 171

Epinephrine is the principal catecholamine involved in metabolic reactions

Back 171

increases inotropic and chronotropic effects and increases venous return to the heart which increases cardiac output and blood pressure. Glucose is preserved for the nervous system by epinephrine as well.

Front 172

Cortisol dec

Back 172

activity of T helper 1 cells

Front 173

Cortisol inc

Back 173

activity of T helper 2 cells

Front 174

Stress-Age Syndrome

Back 174

is what occurs as we age when a set of neurohormonal and immune alterations as well as tissue and cellular changes develop.

Front 175

These age changes include

Back 175

immunodepression, hypercoagulation of blood, free radical damage of cells and others so obviously when dealing with life stessors and the potential for illness in older individuals you may change your plan of care as opposed to dealing with someone younger.