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nurs pathophysiology > rrd 1 > Flashcards

rrd 1 Flashcards

basic concepts, genetic influence in disease, intracellular function and disorders

1
Q

physiology

A

study of functions and processes that occur in body > mostly the normal processes

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2
Q

pathophysiology

A

the study of the underlying changes in body physiology that result from disease or injury

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3
Q

physiologic amenorrhea vs pathophysiological amenorrhea?

A

phys: menstrual flow ceases because of menopause, pregnancy, etc.

pathophys: menstrual flow ceases because of cancer, etc.

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4
Q

homeostasis

A

maintenance of constant conditions in the body’s internal environment

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5
Q

cells must have a constant supply of (1) ______, ______, _____, and exist in narrow (2) ______ and ______ range.

A

(1) nutrients, H2O, O2
(2) pH, temperature

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6
Q

Maintaining homeostasis is essentially a ______ act. Body is always trying to _____ when homeostasis is challenged by changes.

A

balancing, right itself

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7
Q

stressors

A

the challenges to the body’s balance

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8
Q

compensation

A

return to homeostasis after being challenged by a stressor (aka adaptation or healing)

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9
Q

how is compensation achieved?

A

control/compensatory mechanisms

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10
Q

what is the compensatory response when the body is exposed to elevated external temperatures or heavy exercise?

A
  1. Body temperature rises.
  2. The hypothalamus senses the elevated core temperature.

3 (1). The hypothalamus sends a signal to the skin to produce sweat.
4 (1). Heat loss through evaporation

3 (2). dilation of the superficial blood vessels occurs
4 (2). Heated blood circulates from the core to the periphery.
5 (2). Heat loss through radiation (heat removed from body into surrounding air)

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11
Q

what kind of stressor is elevated external temperature or heavy exercise?

A

“normal” daily-life stressors

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12
Q

what is the compensatory response’s MAIN GOAL when you lost a lot of fluid such as blood (massive bleeding) or water (dehydration)?

A

keep the remaining fluid volume circulating as effectively as possible - temporary measures until the cause of the problem is fixed

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13
Q

what is the compensatory response for blood loss?

A
  • HR would increase to get blood around faster to temporarily make up for the loss of volume
  • periphery arteries (arms and legs) would constrict to shunt whatever blood volume is left to the central areas (brain, heart, lungs, kidneys)
  • cool hands and feet
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14
Q

what does it mean when the control mechanisms are exhausted?

A

the body is unable to appropriately meet the challenge of the stressors

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15
Q

what happens when the control mechanisms are exhausted?

A

compensation can deteriorate either rapidly or slowly into decompensation

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16
Q

decompensation

A

failure to compensate, adapt, heal, etc.

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17
Q

disease

A

harmful condition of the body (and/or mind)

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18
Q

disorder

A

distrubance in the healthiness of the body

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19
Q

syndrome

A

collection of symptoms

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20
Q

are disease, disorder, and syndrome interchangeable?

A

for the class, YES

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21
Q

risk factors

A

factors that or contribute to/increase probability that a disease will occur > “setting the stage”

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22
Q

examples of risk factors

A

heredity, age, ethnicity, lifestyle (smoking, eating habits, etc.), environment

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23
Q

precipitating factor

A

a condition or event that triggers a pathologic event or disorder > “kick-off”

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24
Q

etiology

A

the cause of a disease > includes all factors that contribute to the development of the disease

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25
Q

examples of etiology

A
  • etiology of AIDS: HIV
  • etiology of rheumatic heart disease: autoimmune rxn
  • etiology of TB: mycobacterium
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26
Q

idiopathic

A

disease with an unidentifiable cause

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27
Q

iatrogenic problem

A

occurs as a result of a medical treatment

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28
Q

example of iatrogenic problem

A

kidney failure due to improper use of antibiotics prescribed by a healthcare provider
- etiology of the kidney failure was iatrogenic

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29
Q

nosocomial problems

A

result as a consequence of being in a hospital environment

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30
Q

example of nosocomial problem

A

urinary tract infection is an nosocomial infection if it developed while the patient was in the hospital

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31
Q

clinical manifestations (S&S)

A

the demonstration of the presence of a sign and/or symptom of a disease

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32
Q

signs

A

manifestations that can be objectively identified by a trained observer

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33
Q

symptoms

A

subjective manifestations that can only be reported by the person experiencing them - pain, nausea, fatigue

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34
Q

S&S

A

signs and symptoms
- also known as S/S
- “symptoms” is a shortcut in medical vernacular instead of saying signs and symptoms

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35
Q

local S&S

A

redness, swelling, heat, rash, and lymphadenopathy in a particular area

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36
Q

systemic S&S

A

fever, urticaria (hives), malaise (“I feel dragged out” or “awful all over”), systemic lymphadenopathy

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37
Q

acute S&S

A

fairly rapid appearance of S&S of disease (over a day to several)
- usually last a short time

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38
Q

example of acute S&S

A

the patient had acute URI (upper resp infection) that resolved within a few days

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39
Q

acute S&S can also mean what?

A

increase in severity
- ex: The acuity of the patient’s URI increased and he had to be hospitalized.

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40
Q

chronic S&S

A

develop more slowly
- often insidious and last longer
- can wax and wane over months or years

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41
Q

remissions in chronic S&S

A

periods when S&S disappear or diminish significantly (wane)

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42
Q

exacerbations in chronic S&S

A

periods when S&S become worse or more severe (wax)
- ex: The patient had an exacerbation of his chronic asthma and had to go to the hospital.

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43
Q

central location of manifestations

A

refers to a problem/situation that is occurring towards the center/core of the body

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44
Q

what organ systems are being referred to in central location of manifestations?

A

essential organ systems like the brain, heart, lungs, kidneys

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45
Q

example of central location of manifestations

A

when someone loses a lot of blood, the body shunts most of the remaining blood away from non-essential areas (guts, hands, feet) so the essential organs are oxygenated
- most of the blood volume left ends up circulating centrally

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46
Q

the more central an area/problem is, the more _____ to the core it is

A

proximal

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47
Q

example of proximal in a sentence

A

the arm was fractured proximal to the elbow -> break between the elbow and the shoulder

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48
Q

peripheral location of manifestations

A

refers to a problem/situation that is occurring toward the outer parts of the body, away from the core

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49
Q

example of peripheral location of manifestations

A

if there is large blood loss, the blood vessels of the periphery often constrict so that not a lot of blood can circulate in those areas (why a sign of shock is cool, pale extremities)

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50
Q

shock

A

low BP + S&S of not getting enough blood to different parts of the body
- ex: confusion from not getting blood to brain

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51
Q

the more peripheral an area/problem is, or further ____ from the core of the body, the more _____ it is.

A

away, distal

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52
Q

example of distal in a sentence

A

distal to the blood clot in the left coronary artery, the tissue lost oxygenation and died

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53
Q

prognosis

A

predicted outcome of a disease based on certain factors > the usual course of that particular disease

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54
Q

prognosis based on age

A

patients at either end of the age spectrum (infants and elderly) are at a higher risk for a poor prognosis due to immature or worn-out immune systems

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55
Q

prognosis based on presence of comorbidities

A

two or more coexisting medical conditions increases the chance of poor prognosis
- ex: the patient’s comorbidities of heart and lung disease contributed to his poor prognosis in recovering from pneumonia

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56
Q

sequela (plural: sequalae)

A

aftermath of a disease > any abnormal condition that follows and is the result of disease, injury, or treatment
- complications

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57
Q

another term for sequela is?

A

outcome
- ex: a positive sequela of getting pneumonia was that the patient stopped smoking
*sequela is usually used with a negative connotation

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58
Q

the _____ of sequela varies

A

severity

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59
Q

examples of sequelae with various degrees of seriousness

A
  • sequela of rheumatic fever can sometimes be a bad heart valve
  • possible sequela of chicken pox is scarring
  • possible sequela of stroke is weakness on one side of the body
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60
Q

gene

A

segment of DNA molecule that is composed of an ordered sequence of nucleotide bases (adenine, guanine, cytosine, thymine)

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61
Q

main function of genes

A

coding for synthesis of proteins that form our traits and functional characteristics

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62
Q

examples of permanent proteins that genes code for

A
  • eye pigment, hair color, blood type in developing fetus
  • personality and susceptibility to certain diseases
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63
Q

examples of “day-to-day” functional proteins genes code for

A

hormones, antigens, antibodies, enzymes

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64
Q

when there is a _____ of a gene, the ______ it is responsible for often malfunctions

A

mutation, protein

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65
Q

example of a mutation causing protein malfunction

A
  1. gene that codes for lactase mutated
  2. lactase cannot properly breakdown and process lactose
  3. lactose ingestion causes diarrhea
    ^Lactose Intolerance
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66
Q

chromosome

A

rod-shaped body in the nucleus that contains “beads” of DNA information > DNA helix containing genes that take shape of a chromosome

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67
Q

hierarchy of genetic information

A
  1. sequence of nucleotide bases forms a gene
  2. genes make up a DNA molecule
  3. DNA molecule forms into a specialized shape (chromosome)
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68
Q

a person receives ____ chromosomes from each parent, so you end up with ____ pairs or a total of _____.

A

23, 23, 46

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69
Q

how many pairs are autosomal? what does it mean to be autosomal?

A

22 pairs, NON-sex chromosomes

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70
Q

each of the 22 pairs that are autosomal are _________.

A

closely alike

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71
Q

what is the 23rd pair of chromosome?

A

sex chromosomes - XX or XY

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72
Q

the autosomal chromosome pairs each has genes that ______ on the other chromosome.

A

closely match or partners

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73
Q

partner genes have the ______ location (LOCUS) on each respective chromosome and code for the _____ trait.

A

same, same

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74
Q

partner genes on the same location and code for the same trait are?

A

a pair of alleles

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75
Q

difference a pair of alleles can have?

A

one can be dominant, the other recessive (can be both dom or both rec though)

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76
Q

genotypes

A
  • AA, aa, Aa > the notation for dominant/recessive alleles
  • represent what was inherited from mom and dad
  • overall genetic composition
  • refers to a specific set of alleles
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77
Q

AA is?

A

homozygous dominant

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78
Q

aa is?

A

homozygous recessive

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79
Q

Aa is?

A

heterozygous

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80
Q

what would a geneticist use to find the percent chance of two people with certain genotype having a child with certain genetic characters?

A

punnett square

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81
Q

phenotype

A

a person’s observable characteristics (anatomic, physiologic, biochemical, behavioral) as determined by genes and environment

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82
Q

genetic disorders

A

a disease caused by abnormalities in an individual’s genetic material

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83
Q

example of inherited genetic disorders

A

sickle cell disease is caused by an inherited, altered (mutated) gene

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84
Q

example of spontaneous genetic disorders

A
  1. free radicals from as a result of aging
  2. causes damage to the DNA
  3. protein synthesis is altered leading to gene mutations
  4. an “oncogene” develops which causes rapid, wild proliferation of cell growth
  5. cancer may develop
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85
Q

what are other ways to categorize genetic disorders?

A

mitochondrial DNA, multifactoral, chromosomal, single-gene

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86
Q

mitochondrial DNA disorders

A

small bits of DNA are found in the mitochondria
- disorders of this type uncommon

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87
Q

environmental is used to mean?

A

any influence other than inherited

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88
Q

multifactorial genetic disorders

A

combo of environmental triggers and variations/mutations of genes + sometimes inherited tendencies

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89
Q

example of multifactorial genetic disorders involving lung cancer

A
  1. smoke and toxins irritating bronchial tissue
  2. one or more genes in cells of tissue deranged - oncogenes created
  3. code for wild, uncontrolled growth of cells
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90
Q

what are other examples of multifactorial genetic disorders?

A
  • hypertension (HTN)
  • coronary artery disease (CAD)
  • diabetes mellitus (DM)
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91
Q

teratogen

A

any influence (drugs, radiation, viruses, etc.) that can cause congenital defects

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92
Q

congenital defects

A

abnormalities that are either detectable at birth and/or can be attributed to fetal development “glitches”

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93
Q

examples of teratogenic disorders/congenital defects

A
  • FAS (fetal alc syndrome) -> toxicity of alc causes gene mutations during gestational development
  • thalidomide babies -> born with abnormal arms and legs due to moms taking thalidomide for nausea during early pregnancy
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94
Q

chromosomal disorders (chromosomal aberrations)

A

type of genetic disorders that result from:
1. alterations to the numbers/structures of a chromosome
2. alters local genes (genes in immediate area)
3. gene’s functionality disrupted
4. genes don’t code for protein correctly
5. rise of phenotype of the disorder

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95
Q

example of chromosomal disorder due to alteration to numbers of chromosome

A

Down’s syndrome - disorder of numbers of chromosomes and sometimes associated with pregnancies of women > 35 yrs old

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96
Q

Down’s syndrome is a glitch that occurs in very early ______ division and chromosomal distribution of a __________

A

cellular, fertilized egg

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97
Q

how many chromosomes does a fetus end up when experiencing the glitch associated with Down’s syndrome?

A

47 chromosomes (instead of 46)

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98
Q

where does the extra chromosome occur with Down’s syndrome?

A

at site #21 - the 21st chromosome set comes with 3 instead of 2

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99
Q

another name for the 21st chromosome associated with Down’s syndrome

A

trisomy 21

100
Q

phenotype of trisomy 21

A
  • mental retardation
  • low-set ears
  • epicanthic fold to eyes
  • short limbs
  • larger-than-normal tongue
101
Q

some types of chromosomal aberrations are caused by alterations of chromosomal _______, such as deletion, duplication, rearrangement of gene sites (______) on the chromosome

A

structure, translocation

102
Q

example of chromosomal disorder due to alterations to chromosome structure

A

Philadelphia chromosome

103
Q

Philadelphia chromosome

A

results from translocation

104
Q

polysomy

A

more chromosomes than normal
- ex: Down’s

105
Q

single-gene disorders

A
  • due to an inherited mutated gene
  • mutated gene causes abnormal protein that cannot carry out its normal function -> disorder
106
Q

patterns of single-gene disorders

A

autosomal recessive, autosomal dominant, sex-linked

107
Q

autosomal recessive disorder

A

mutated (diseased), recessive (weak) gene partners up with an allele that is also recessive and diseased, causing the protein they code for to malfunction -> abnormality/disease/disorder will occur based on bad protein

108
Q

example of an autosomal recessive disorder

A

sickle cell anemia

109
Q

sickle cell anemia genotype development

A
  • @ certain locus on certain pair of chromosomes, a pair of alleles has job of coding for normally shaped Hgb
  • during fertilization: person inherits the sickle-cell disease gene from mom and dad (recessive, mutated Hgb-coding gene)
  • homozygous recessive genotype: dd
110
Q

sickle cell patho development

A
  • abnormal-shaped Hgb (sickle-shaped) makes RBC sickle-shaped
  • RBCs more susceptible to damage as they move thru blood stream -> less than normal #s of RBCs (anemia)
111
Q

sickle cell anemia phenotype (S&S caused by geno and patho development)

A

SOB (shortness of breath), weakness & fatigue, and ischemic pain

112
Q

what is SOB, weakness & fatigue by sickle cell anemia specifically due to?

A

decreased O2 being carried to tissues of the body

113
Q

the decreased capacity of O2 being carried to the tissue of the body in context of sickle cell anemia is because of?

A
  • anemia: less #s of RBCs to carry Hgb which in turn carries O2
  • deformed Hgb cannot carry usual #s of O2 molecules
114
Q

what is ischemic pain from sickle cell anemia caused by?

A

*especially in joints
- deformed RBCs clog up capillaries that usually carry O2-rich blood to tissues
- distal tissues starved to O2 and “cry out” in pain (womp womp)

115
Q

ischemia / ischemic pain

A
  • cells not getting enough O2 due to circulatory malfunction
  • pain in the tissue that is not getting enough oxygen
116
Q

genotype of person who inherits a sickle-cell disease gene from one parent but a NORMAL Hgb-coding gene from the other parent?

A

Dd

117
Q

a person that has a heterozygous genotype for sickle cell anemia is considered a ______ because?

A

carrier, does not have the disease but has the gene for it to carry to offspring

118
Q

T/F a carrier can have a milder phenotype of the disease (mild S&S) - “having the trait”

A

TRUE

119
Q

in context to sickle-cell anemia, a person that is DD is considered?

A

homozygous normal - do not have to worry about having/passing the disease

120
Q

autosomal dominant disorders

A
  • when a person inherits a mutated, diseased gene that is dominant
  • gene that codes for disease dominant while gene that codes for normal is recessive
121
Q

example of autosomal dominant disorder

A

polycystic kidney disease (PKD)

122
Q

genotype development of PKD

A
  • @ certain locus on certain pair of chromosomes, pair of alleles code for normal kidney tissue
  • during fertilization: person inherits mutated kidney tissue gene that codes for abnormal kidneys
  • even when mutated gene is paired with normal allele, it will override normal allele’s coding
123
Q

patho development of PKD

A

kidney tissue develops cysts, which can reduce various kidney fxns and lead to kidney failure as person goes thru life

124
Q

genotype notation for PKD

A

PP or Pp

125
Q

what is the genotype notation for a person that does not have PKD? what is it called?

A

pp, homozygous recessive

126
Q

S&S of PKD

A
  • hematuria (blood in urine), proteinuria, frequent kidney infections
  • pain at costovertebral angles and abdomen
  • kidney stones
127
Q

recombinant DNA

A

a form of genetic engineering

128
Q

recombinant DNA is _____ DNA that results from purposefully combining two or more _______ sources of DNA

A

new, different

129
Q

example of recombinant DNA engineering

A

altering DNA codons in bacteria to make proteins that bacteria would not ordinarily produce

130
Q

current applications of recombinant DNA process

A
  • human GH for children lacking it
  • exogenous (from outside the body) insulin for diabetics
  • factor VIII for hemophiliacs
  • drugs (tPA & tenecteplase) given as clot-busters in patients having MI (myocardial infarction: clot in coronary artery, blocking blood flow to distal tissue)
131
Q

many normal daily changes in body _________ can affect the metabolic pathway and usually, the body can adjust and maintain ___________. ongoing ________.

A

homeostasis, equilibrium, fine-tuning

132
Q

when there are problems that disrupt homeostasis of cellular metabolism and the provision of ATP for body needs, what happens to the body?

A

more difficult for the body to adjust and return to equilibrium

133
Q

many disorders and diseases processes either ______ or are ______ some sort of cellular-level disruption that eventually leads to a decrease in ______.

A

cause, caused by, ATP

134
Q

etiology of cellular disruptions include:

A
  • hypoxia
  • nutritional problems
  • changes in balance of electrolytes and other solutes (acid/base imbalance)
  • changes in fluid distribution
135
Q

hypoxia

A

decrease in amt of oxygen to cell or ability to use oxygen appropriately

136
Q

example of nutritional problems that can cause cellular disruptions

A
  • decreased glucose
  • vitamin availability for cell use
137
Q

hypoxia has a spectrum of?

A

etiology and seriousness
- overworked muscles in extreme exercise (muscle use up immediate avail O2)
- difficulty breathing and can’t get enuf O2 to heart to circulate to tissues
- artery in arm cut so tissues distal to trauma cannot get O2

138
Q

if there is hypoxia, cellular metabolism has to recycle through ________ rather than continue down the usual aerobic pathway.

A

glycolysis

139
Q

why does cellular metabolism use glycolysis during hypoxia?

A

glycolysis is the only step that can operate under normal, aerobic conditions and anaerobic conditions

140
Q

positive side of anaerobic glycolysis

A
  • give 2 ATP per glucose molecule to give energy to cell
  • temp stop-gap measure to keep body going until cells can get more O2 and reestablish aerobic metabolism
141
Q

negative side of anerobic glycolysis

A
  • 2 ATP not enough to keep going for a long time
  • every time metabolic process must recycle thru glycolysis -> multiple pyruvate (pyruvic acid) accumulate -> acidosis
142
Q

acidosis

A

state of greater-than-usual concentration of acidic substances in the blood and cells

143
Q

two main sequela result from hypoxia

A
  • deficiency of ATP for cellular fxns
  • altered acid/base balance
144
Q

hypoxia can cause?

A

damage and death to tissue

145
Q

example of deficiency of ATP for cellular fxns due to hypoxia

A

w/o ATP, Na/K pump of each cell cannot maintain normal electrical cell membrane status + propagation of electrical impulses will be disrupted

146
Q

example of altered acid/base balance due to hypoxia

A

acidosis can tip body pH out of its narrow, desirable range quickly

147
Q

glycogen

A
  • molecule too large to be used for energy as is
  • can be stimulated to break down into small glucose molecules that can be used for energy
  • stored glucose
148
Q

glucose

A

obtained from carbohydrates to begin cellular metabolic pathway that leads to ATP

149
Q

vitamins

A

provide support staff for metabolic pathway (along with other substances)

150
Q

process of glucose access and usage depends on ______________ at any given moment

A

cellular metabolic needs

151
Q

if you have just eaten and have normal glucose system, what happens with your glucose levels? what is triggered?

A
  1. glucose levels in blood normally goes up - temp hyperglycemia state
  2. pancreas triggered to secrete insulin to circulate to cells
  3. insulin assist in getting glucose molecules from blood into cell to use as main source of cellular energy
152
Q

if intake of food/glucose is ______ than immediate cellular energy needs, insulin directs the ______ glucose to be stored as glycogen in the liver. what is this called?

A

greater, excess, glycogenesis

153
Q

insulin triggers ________ building up process of 1). ______ entering cells and 2). creation of ______ (glycogenesis)

A

regulatory, glucose, glycogen

154
Q

if you don’t eat and/or the availability of glucose is less than cellular energy needs a state of __________ (low blood sugar) usually exist.

A

hypoglycemia

155
Q

what hormones are triggered by low blood glucose?

A

counterregulatory hormones

156
Q

counterregulatory hormones are also called ____ because?

A

stress hormones because hypoglycemia is stressful for the body - they come to the rescue

157
Q

what hormones are counterregulatory hormones?

A
  • epinephrine from the adrenal medulla
  • cortisol from the adrenal cortex
  • growth hormone (GH) from the pituitary
  • glucagon from the pancreas
158
Q

what roles do the counterregulatory hormones have with hypoglycemia?

A
  • alarms: sensations of hunger, shakiness, sweating, irritability telling you to EAT
  • stimulate backup plan #1: glycogenolysis if you don’t eat
159
Q

glycogenolysis

A
  • conversion of glycogen to glucose for energy use in cells
  • corrects hypoglyemia, results in higher blood sugar
  • stop-gap measure until we can take in glucose
160
Q

if glucose is either unavailable/cannot get into the cell to participate in metabolic pathway + glycogenolysis already exhausted person’s glycogen store, what happens?

A

gluconeogenesis (backup plan #2)

161
Q

gluconeogenesis

A
  • break down fats and protein
  • use of any other substances besides carbohydrates for cellular energy
162
Q

what is one of the breakdown products of fats and proteins?

A

ketones

163
Q

good characteristic of ketones

A

offer body some energy - usually enuf to be a stop-gap until glucose is available

164
Q

bad characteristics of ketones

A
  • acids: over time, danger of acidosis
  • can’t be used by brain cells - brain cells must have glucose for energy
165
Q

dizzy, dull-witted, or cognitively challenged when hypoglycemic, what is happening? clinical significance?

A

brain cells are reliant on glucose for energy
- when deprived, become electrically disturbed
- can lead to unconsciousness, seizure, and/or death
- test blood sugar if patient presents with altered level of consciousness

166
Q

glycogenolysis and gluconeogenesis are considered to be ___________, ___________ processes triggered by counterregulatory hormones when hypoglycemia is present.

A

breaking-down, counterregulatory

167
Q

examples of disease processes related to cellular metabolism “back-up plans”

A
  • glycogen storage diseases
  • Type 1 diabetes
168
Q

glycogen storage diseases

A

abnormalities in glycogenesis or glycogenolysis

169
Q

example of glycogen storage disease

A

McArdle’s disease
- autosomal recessive disease in which normal ability to breakdown glycogen (glycogenolysis) is diminished

170
Q

S&S of McArdle’s disease

A

muscle weakness and cramps during exercise bc no energy reserves

171
Q

type 1 diabetes

A

gluconeogenesis taken to extreme
1). can’t make insulin
2). no insulin, glucose cannot get into cell
3). blood glucose level rise
4). body turns to sustained gluconeogenesis as main energy pathway
5). ketone overaccumulation in blood = hyperketonemia

172
Q

hyperketonemia manifested/seen in tests by?

A
  • blood test showing high serum ketones
    AND ONE OF THE FOLLOWING:
  • blood test showing low (< 7.35) blood pH (ketoacidosis)
  • urine test showing ketonuria (ketones spill into urine)
  • S&S like acetone breath (excretion via lungs)
173
Q

how does alterations in vitamin and mineral access or usage contribute to disruption in metabolic pathway?

A
  • vitamins + minerals necessary to maximize ATP creation (need only small amts but is crucial for well-being)
  • sufficient amts cannot be made by our body, so have to be supplied by diet
  • vitamin deficiencies due to lack of availability of certain foods, poor dietary habits, and/or chronic disease
174
Q

what is an example of a type of patient nurses often see who would be high risk for vitamin deficiencies?

A

an alcoholic

175
Q

the byproducts of the body’s normal metabolic activities are slightly more ________ than ______. to counteract that _____ tendency, the body likes to keep a very narrow and slightly ______ pH range of blood, which is _____.

A

acidic, alkaline, acidic, alkaline, 7.35 - 7.45

176
Q

often an alcoholic has very _____ diet - obtains ______ iron and B vitamins such as thiamine (and other ______)

A

poor, minimal, deficiencies

177
Q

sequela of iron deficiency

A
  • iron-deficiency anemia
  • S&S related to low ATP and low oxygenation: weakness, fatigue, SOB
178
Q

thiamine deficiency is called _____ and sequelae include _____ problems

A

beriberi, neuro

179
Q

beriberi is the disease name of general thiamine deficiency. what is the group of neurologic S&S especially see in in alcoholics with beriberi?

A

Wernicke-Korsakoff syndrome

180
Q

how does Wernicke-Korsakoff syndrome manifest?

A

memory loss and ataxia (staggering, uncoordinated gait)

181
Q

____ is important in neurologic cell functioning. many S&S of depletion of this vitamin show up as ______ problems such as _____ and _____.

A

B1, neurologic, Wernicke-Korsakoff syndrome, paresthesia

182
Q

paresthesia

A

numbness and tingling or other unusual sensations, usually in legs
- pins and needles feeling

183
Q

T/F some medicinal & street drugs generally don’t interfere with vitamin absorption

A

FALSE

184
Q

what poison can contribute to disruption in metabolic pathway?

A

cyanide
- present in insecticides, rodenticides, metal polish, burning wool, certain drugs (like nitroprusside)
- considered potential bioterrorism drug

185
Q

S&S of poison toxicity

A

headache, agitation, confusion, vomiting, eventually resp problems, death

186
Q

mechanism of action for poison disrupting metabolic pathway

A

inhibits cytochrome oxidase

187
Q

homeostasis of solutes in the body means what?

A

there are approx the same sum of ions & other solutes inside each fluid compartment compared to the compartment “next door”

188
Q

alteration in the solution composition in one compartment, a ________ begins

A

domino effect

189
Q

what is the domino effect beginning when there is an alteration in the solution composition in one compartment referring to?

A

diffusion of solute particles resulting in changes in the next compartment, then the next, etc.

190
Q

why does diffusion of solute particles occur in the following compartments?

A

body is always striving to return to normal/homeostatic composition of solutes in each compartment

191
Q

changes in solute and fluid balance occurs first in the _____ then spreads to the _______.

A

plasma compartment (blood), tissue (interstitial fluid and cells)

192
Q

_____ exist until body can right itself or get medical intervention as needed

A

changes/imbalances

193
Q

therapeutic example of the domino effect of solute shifts from compart to compart

A

1). take K+ pills, digested and absorbed into blood vessels in lining of stomach + duodenum
2). K+ enters blood steam and increases K+ level -> electrolyte imbalance
3). blood circulates to various tissues
4). K+ eventually diffuse into tissue bc tissue has less K+ than blood

194
Q

hyperkalemia

A

higher-than-normal numbers of K in blood

195
Q

hypokalemia

A

lower-than-normal numbers of K in bloodh

196
Q

hypernatremia

A

high Na+ in blood

197
Q

hyponatremia

A

low Na+ in blood

198
Q

hypercalcemia

A

high Ca2+ in blood

199
Q

hypocalcemia

A

low Ca2+ in blood

200
Q

normal electrical status exists when there is a normal distance (_________) between the two poles of:

A

polar gap status
- RMP of -90 mV
- goal charge of +30 mV (charge need for cell to contract/work)

201
Q

what is affected when a disorder/disease/situation disrupts the normal balance of electrolytes in the blood?

A

balance of cations and anions in the tissue cells will be affected

202
Q

the balance of cations/anions in the tissue cells causes the ______ of the cells’ RMP to a more positive # or less positive #

A

resetting

203
Q

hypopolarization

A

RMP is reset to a MORE positive number than normal
- shorten polar status

204
Q

hyperpolarization

A

RMP is reset to a LESS positive number than normal
- lengthen polar status

205
Q

hypopolarized states

A

situations in which cell membranes have been reset to a MORE positive number than normal
- shortening polar gap status
- more sensitive

206
Q

examples of states which cells become hypopolarized

A
  • hypocalcemia
  • hyperkalemia
  • hypernatremia
207
Q

general concept of hyperkalemia and hypernatremia causing hypopolarization

A

more cations (+) in the blood means that eventually, more cations will diffuse from the blood INTO cells

208
Q

steps for hyperkalemia and hypernatremia causing hypopolarization

A

1). more cations in blood
2). cations diffuse from blood into cells
3). more positive state within the cell
4). cell membrane reset to more positive RMP
5). polar gap has shortened - less distance for cells’ change to get to depolarization point when stimulated by incoming electrical signal
6). increased sensitivity and quicker to contract/work

209
Q

how does hypocalcemia cause hypopolarization?

A
  • presence of low calcium levels in blood as blood circulates tissue beds triggers an INCREASE in permeability of cell membranes to Na+
  • MORE Na+ allowed INTO the cell than normal
  • more cations into cell causes increased positivity
210
Q

S&S of hypopolarization

A
  • muscles that are too sensitive (hyperactive, irritable)
  • contact with smaller-than-normal stimulation, result in muscle tics or spasms (positive Chvostek’s sign)
  • severe and/or unrelenting spasms is tetany
211
Q

hyperpolarized states

A

situations in which cell membranes have been reset to a LESS positive number than normal
- lengthen polar gap status
- less sensitive

212
Q

examples of states in which cells become hyperpolarized

A

hypercalcemia, hypokalemia, hyponatremia

213
Q

general concept of hypokalemia and hyponatremia causing hyperpolarization

A

less cations in the blood, eventually more cations will diffuse OUT of the cells INTO the blood

214
Q

steps for hypokalemia and hyponatremia causing hyperpolarization

A

1). less cations in blood
2). more cations diffuse out of cell into blood
3). less positive state within the cell since cations moved out
4). cell membrane reset to less positive RMP
5). cell hyperpolarized
6). more distance for cells’ charge to get to depolarization point when stimulated by incoming electrical signal
7). less sensitive - takes longer for cell to contract

215
Q

hypercalcemia causes hyperpolarization how?

A

1). high calcium levels in blood as blood circulates in tissue beds
2). decrease in permeability of cell membranes to Na+
3). less Na+ allowed into the cell than normal
4). decreased cations in cell
5). decreased positivity

216
Q

S&S of hyperpolarization

A
  • muscles less sensitive than usual (hypoactive)
  • contract more slowly
  • fatigue, lethargy, mental slowness
217
Q

ABGs stand for? what is it?

A

arterial blood gases: a measurement of oxygenation and acid/base balance in blood

218
Q

CO2 and H+ in context of pH are?

A

acidic

219
Q

HCO3 (bicarbonate) in context of pH is?

A

alkaline

220
Q

too much CO2/H+ or too little HCO3?

A

acidosis

221
Q

too little CO2/H+ or too much HCO3?

A

alkalosis

222
Q

lungs control what gas? what do they have little control over?

A

CO2, HCO3

223
Q

what organ rules over HCO3 and H+?

A

kidneys

224
Q

pH normal range

A

7.35-7.45

225
Q

HCO3 normal range

A

22-28

226
Q

pCO2 normal range

A

35-45

227
Q

pO2 normal range

A

80-100

228
Q

SaO2 normal range

A

97-100%

229
Q

acidosis

A
  • most often clinically measured as part of ABGs: blood pH is < 7.75
230
Q

body needs narrow range of slightly ______ to counteract an overall tendency of metabolic activates towards ______, which is a state not tolerated by the body

A

alkaline, acidosis

231
Q

S&S of acidosis

A
  • headache, disorentation
  • nausea, vomiting
  • muscle pain, cramps
  • SOB, low BP, shock
  • organ fail, death
232
Q

metabolic acidosis

A
  • acid/base imbalance releated to problem in the kidneys and/or any other disorder/body system except lungs
  • low pH and low HCO3
233
Q

metabolic acidosis is caused by a metabolic problem that results in one or more of what?

A
  • excess accumulation of H+ (and other acids) in body
  • not enough excretion of H+ in the urine
  • not enough HCO3 being made
  • too much HCO3 being excreted in the urine
234
Q

example of metabolic acidosis etiology

A

1). available O2 in muscle used up from exercising too hard
2). hypoxia in tissue - anaerobic glycolysis for energy needs
3). pyruvate molecules created during glycolysis converted to lactic acid (full of H+)
4). lactic acid can convert to glucose in liver for emergency
5). too much lactic acid either locally or systemically become irritating to tissue and/or organ system

235
Q

other examples of processes that may result in metabolic acidosis

A
  • kidney failure: sick kidneys can’t excrete H+ or make HCO3 -> acid accumulation
  • diabetic ketoacidosis: ketones accumulated bc body sustained gluconeogenesis
  • posions, drug overdose, alc: breakdown products are acidotic
236
Q

compensation for metabolic acidosis

A
  • primary means via lungs
  • lungs try to decease acids by INCREASING amt of CO2 EXHALED
  • increase rate and/or depth of respirations
237
Q

respiratory acidosis

A

state of low pH caused by ventilation problem such as diminished effectiveness of breathing or decreased resp rate

238
Q

respiratory acidosis results in what?

A

retention of CO2 (acid accumuation)

239
Q

respiratory acidosis is compensated by what?

A

kidneys: HCO3 production by the kidneys increased to buffer situation/counteract acid

240
Q

alkalosis

A
  • blood pH > 7.45
  • less common than acidosis
  • high pH and high HCO3
241
Q

etiology of metabolic alkalosis

A
  • excess accumulation of HCO3 in the body
  • not enough excretion of HCO3 in the urine
  • too much acid (H+ and others) being excreted in urine or lost in other metabolic ways
  • not enough acid being made
242
Q

causes of metabolic alkalosis

A
  • large amount of vomiting
  • over-ingestion of bicarbonate (HCO3)
243
Q

compensation of metabolic alkalosis

A

via lungs - decease rate and depth od respirations

244
Q

respiratory alkalosis

A

state of high pH caused by hyperventilation
- increase rate of breathing = blowing off more CO2 = less CO2 in blood = higher pH

245
Q

example of a cause of respiratory alkalosis

A

anxiety - when anxious, begin hyperventilating

246
Q

compensation of respiratory alkalosis

A

kidneys, decrease amt of of HCO3 made or increase excretion

nurs pathophysiology (13 decks)

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