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312 Patho > PATHO FINAL > Flashcards

PATHO FINAL Flashcards

1
Q

FUNCTIONS OF THE ENDOCRINE SYSTEM

A

COMMUNICATION SYSTEM THAT USES CHEMICAL MESSENGERS OR HORMONES THAT HELP US TO TRANSMIT INFO FROM CELL TO CELL OR ORGAN TO ORGAN

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2
Q

HORMONES

A

CHEMICAL MESSENGERS

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3
Q

WHAT DOES THE ENDOCRINE SYSTEM OVERLAP WITH

A

NERVOUS SYSTEM AND IMMUNE SYSTEM
*TERMS LIKE NEUROENDOCRINE IMMUNE SYSTEM

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4
Q

WHAT DOES THE ENDOCRINE SYSTEM DO

A
  1. GROWTH AND DEVELOPMENT
  2. SEX DIFFERENTIATION- REPRODUCTION
  3. METABOLISM-DIGESTION, USE AND STORAGE OF NUTRIENTS, REGULATION OF SOME ELECTROLYTES AND FLUIDS
  4. ADAPTATION TO AN EVERY CHANGING ENVIRONMENT- HOMEOSTASIS
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5
Q

HOW DO HORMONES FUNCTION AS CHEMICAL MESSENGERS

A

MOVE THROUGH BLOOD TO DISTANT TARGET SITES OF ACTION.
CAN ACT LOCALLY AS PARACRINE OR AUTOCRINE MESSENGERS
MOST ARE PRESENT IN BODY FLUIDS AT ALL TIMES IN VARYING AMOUNTS

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6
Q

CHARACTERISTICS OF HORMONES

A

SINGLE HORMONE CAN EXERT VARIOUS EFFECTS IN DIFFERENT ISSUES–> ESTRODIAL—FROM OVARY BUT DOES THINGS IN ALL KINDS OF TISSUES

SINGLE FUNCTION CAN BE REGULATED BY SEVERAL HORMONES-LIPOLISIS- BREAKDOWN OF FAT— TAKES SEVERAL HORMONES

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7
Q

RECEPTORS ON CELL (SURFACE OR INTRACELLULAR) REACT

A

TO HORMONE TO PRODUCE EFFECT

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8
Q

WHERE ARE HORMONES RELEASED

A

ENDOCRINE GLANDS
1. PITUITARY GLAND
2. THYROID GLAND
3. ADRENAL GLAND
4. PANCREAS

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9
Q

CLASSES OF HORMONES

A

AMINES
AMINO ACIDS
PEPTIDES
POLYPEPTIDES
PROTEINS
STEROIDS
FATTY ACIDS

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10
Q

PARACRINE HORMONES

A

ACT LOCALLY
DO NOT ENTER THE BLOOD STREAM
EX: SEX HORMONES ON THE OVARY

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11
Q

AUTOCRINE

A

PRODUCES SOME KIND OF BIOLOGIC EFFECT ON THE CELL THAT ACTUALLY PRODUCES IT
*EX: INSULIN EFFECT ON PANCREAS BECAUSE THEY ACT ON THE SAME PANCREATIC CELLS

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12
Q

RELEASING HORMONES FROM THE HYPOTHALAMUS DO WHAT

A

TELL THE PITUITARY WHAT TO RELEASE INTO THE BLOOD

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13
Q

BESIDES RELEASING HORMONES, WHAT ELSE CAN THE HYPOTHALAMUS RELEASE

A

PITUITARY INHIBITING HORMONES

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14
Q

HORMONES FROM THE PITUITARY TELL SPECIFIC PERIPHERAL GLANDS TO WHAT

A

GROW AND PRODUCE THEIR HORMONES

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15
Q

HYPOTHALAMUS-PITUITARY-TARGET CELL SYSTEM

A

HYPOTHALAMUS –> RELEASING HORMONES OR PITUITARY INHIBITING HORMONES –> TELL PERIPHERAL GLANDS TO PRODUCE HORMONES

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16
Q

ROUTE OF THE HYPOTHALAMUS PITUITARY TARGET CELL SYSTEM

A

CNS INPUT
HYPOTHALAMUS
RELEASING HORMONE
ANTERIOR PITUITARY
TROPIC HORMONE
TARGET GLAND
HORMONE
TARGET CELL
PHYSIO EFFECT

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17
Q

EXAMPLES OF HORMONES WITH 24 HR FLUCTUATION

A

THOSE THAT REGULATE OUR SLEEP/WAKE CYCLE

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18
Q

EXAMPLES OF HORMONES WITH A 28 DAY PERIOD

A

MENTAL CYCLE

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19
Q

HOW IS HORMONE SECRETION MOST OFTEN REGULATED

A

NEGATIVE FEEDBACK THAT MONITOR SUBSTANCES AND STIMULI IN THE BODY TO PRODUCE A RESPONSE

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20
Q

WHAT IS THE MASTER GLAND AND WHY

A

PITUITARY GLAND
CONTROL THE FUNCTION OF THE MAJORITY OF OUR TARGET ENDOCRINE GLANDS AND CELLS

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21
Q

WHAT DO TROPIC HORMONES DO

A

STIMULATE OR INHIBIT THE TARGET GLAND THEY ARE LOOKING AT

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22
Q

HOW IS THE PITUITARY GLAND DIVIDED

A

ANTERIOR AND POSTERIOR

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23
Q

WHAT DOES THE ANTERIOR PITUITARY RELEASE

A

ADH
OXYTOCIN

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24
Q

WHAT DOES THE POSTERIOR PITUITARY GLAND RELEASE

A

GROWTH HORMONES
TSH
ADRENOCORTICOTROPIC HORMONE
FOLLICLE STIMULATING HORMONE
LUTENIZING HORMONE
PROLACTIN

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25
Q

FEEDBACK REGULATION

A

SENSORS IN THE BODY DETECT A CHANGE AND ADJUST HORMONE SECRETION TO MAINTAIN BLOOD LEVELS

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26
Q

NEGATIVE FEEDBACK

A

DECREASE OF HORMONE LEVELS IN THE BLOOD THAT STIMULATES THE ENDOCRINE CELL TO INCREASE HORMONE PRODUCTION
BLOOD LEVEL RISES PRODUCING SOME KIND OF ACTION ON THE TARGET CELL
AFTER ACTION, THE SENSORS WILL START TO DECREASE

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27
Q

EXAMPLE OF NEGATIVE FEEDBACK SYSTEM

A

THYROID RELEASING HORMONE AND THYROID STIMULATING HORMONE THAT HELP PROMOTE T3 AND T4
INCREASE IN T3 AND T4 CAUSES RELEASE THAT SHUTS DOWN OR SLOWS DOWN THE THYROID

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28
Q

POSITIVE FEEDBACK SYSTEM

A

RISING LEVEL HORMONE THAT CAUSES ANOTHER HORMONE TO RELEASE THAT STIMULATES THE FIRST
CONTINUED RISE IN THE HORMONE LEVEL AND SOMETHING HAS TO ACT TO SHUT THIS OFF

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29
Q

EXAMPLE OF POSITIVE FEEDBACK

A

ESTRODIAL DURING MENSTRUAL CYCLE CAUSES INCREASE IN FSH PRODUCTION WHICH INCREASES ESTRODIAL UNTIL WE HAVE THE DEMISE OF THE UTERINE FOLLICLE
THAT DEMISE IS THE STIMULUS THAT SHUTS OFF THE RISE

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30
Q

ALTERED ENDOCRINE FUNCTION

A

HYPOFUNCTION
HYPERFUNCTION
HORMONE RECEPTOR RESISTANCE

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31
Q

ENDOCRINE HYPOFUNCTION

A

CONGENITAL DEFECTS
GLAND DESTRUCTION

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32
Q

CONGENITAL DEFECTS

A

ABSENCE OF OR IMPAIRED FUNCTION
ABSENCE OF ENZYME NEEDED TO MAKE HORMONES

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33
Q

GLAND DESTRUCTION

A

DECREASED BLOOD FLOW, INFECTION, INFLAMMATION, AUTOIMMUNE RESPONSES, TUMORS

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34
Q

HORMONE RECEPTOR RESISTANCE

A

ABSENCE OF RECEPTORS
DEFECT IN RECEPTOR BINDING

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35
Q

ENDOCRINE HYPERFUNCTION

A

EXCESSIVE STIMULATION AND HYPERPLASIA OF THE GLAND
HORMONE PRODUCING TUMOR
ADMIN OF EXOGENOUS HORMONES

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36
Q

HOW ARE ENDOCRINE DISORDERS CLASSIFIED

A

PRIMARY
SECONDARY
TERTIARY
*DEPENDING ON LOCATION OF DYSFUNCTION IN THE HPT ORGAN SYSTEM

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37
Q

TERTIARY

A

DYSFUNCTION IN STIMULATION FROM THE HYPOTHALAMUS

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38
Q

SECONDARY

A

DYSFUNCTION IN STIMULATION FROM THE PITUITARY

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39
Q

PRIMARY

A

DYSFUNCTION IN THE TARGET ORGAN/GLAND

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40
Q

WHAT HORMONES GENERALLY COME FROM THE HYPOTHALAMUS

A

RELEASING HORMONES, BUT SOME HAVE INHIBITORY PROPERTIES

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41
Q

WHAT IS THE PRIMARY JOB OF THE HORMONES COMING FROM THE HYPOTHALAMUS

A

STIMULATE THE PITUITARY TO RELEASE TROPIC HORMONES

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42
Q

GHRH

A

GROWTH HORMONE RELEASING HORMONE

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43
Q

TRH

A

THYROTROPIN RELEASING HORMONE

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44
Q

CRH

A

CORTICOTROPIN RELEASING HORMONE
AIDS IN RELEASE OF HORMONES FROM ADRENAL CORTEX

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45
Q

GRH

A

GONADOTROPIN RELEASING HORMONE

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46
Q

HYPOTHALAMIC HORMONES

A

GHRH
TRH
CRH
GRH
SOMATOSTATIN
DOPAMINE

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47
Q

SOMATOSTATIN

A

INHIBITORY HORMONE
INHIBITS GHRH AND TSH
DELAYS INTESTINAL ABSORPTION OF GLUCOSE

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48
Q

DOPAMINE

A

INHIBITORY HORMONE
INHIBITS PROLACTIN, FSH, LUTEINIZING HORMONE

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49
Q

POTERIOR PITUITARY HORMONES

A

ADH
OXYTOCIN

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50
Q

ADH

A

INCREASE REABSORPTION OF WATER AND SODIUM BY THE KIDNEY THUS INCREASING OUR VASCULAR VOLUME AND OUR OXYTOCIN

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51
Q

OXYTOCIN

A

STIMULATES UTERINE CONTRACTIONS IN PREGNANT WOMEN
MILK PRODUCTION AFTER CHILDBIRTH

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52
Q

ANTERIOR PITUITARY HORMONES

A

GH
FSH
LH
TSH
ACTH

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53
Q

GH

A

GROWTH HORMONE
STIMULATE GROWTH OF BONE AND MUSCLE
PROMOTES PROTEIN SYNTHESIS AND FAT METABOLISM
DECREASES CARB METABOLISM

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54
Q

FSH

A

FOLLICLE STIMULATING HORMONE
STIMULATES THE GROWTH OF THE OVARIAN FOLLICLE AS WELL AS OVULATION
IN MEN, IT STIMULLATES SPERM PRODUCTION

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55
Q

LH

A

LUTEINIZING HORMONE
WOMEN-STIMULATE OOCYTE, PRODUCTION OF ESTROGEN, AND PROGESTERONE
MEN- DEVELOPMENT OF TESTI TISSUE, STIMULATE SECRETION OF TESTOSTERONE

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56
Q

TSH

A

THYROID STIMULATING HORMONE
STIMULATES THE SYNTHESIS AND SECRETION OF OUR THYROID HORMONES

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57
Q

ACTH

A

ADRENOCORTICOTROPHIC HORMONE
STIMULATES THE SYNTHESIS AND SECRETION OF OUR ADRENAL CORTICAL HORMONES

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58
Q

GH SECRETION IS STIMULATED BY

A

HYPOGLYCEMIA
FASTING
STARVATION
STRESS

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59
Q

GH INHIBITED BY

A

INCREASED GLUCOSE
FREE FATTY ACID RELEASE
OBESITY
CORTISOL

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60
Q

GH IS ALSO KNOWN AS

A

SOMADOTROPIN

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61
Q

WHAT DOES GH DO

A

LATERAL BONE GROWTH
METABOLISM
CARTILAGE GROWTH

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62
Q

WHAT IS THE GROWTH HORMONE RELEASING HORMONE

A

GHRH

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63
Q

WHAT IS OUR GH INHIBITING HORMONE

A

SOMATOSTATIN

64
Q

ACTS OF GROWTH HORMONE

A

GROWTH PROMOTING ACTIONS
ANTI-INSULINE EFFECTS
*ACTS ON THE LIVER
DOESN’T DIRECTLY CAUSE BONE GROWTH

65
Q

WHAT DOES THE LIVER PRODUCE FOR BONE GROWTH WHEN STIMULATED BY GH

A

IGF

66
Q

IGF

A

PEPTIDE THAT ACTS ON CARTILATE AND BONE TO PROMOTE THEIR GROWTH
*WILL SEE LINEAR (HEIGHT) GROWTH, INCREASED SIZE AND FUNCTION IN ORGANS, INCREASE IN LEAN MUSCLE MASS

67
Q

ANTI-INSULIN EFFECTS OF GH

A

ACTION ON OUR ADIPOSE TISSUE (LYPOLISIS, INCREASE IN FFA TO DECREASE FAT TISSUE), AND CARB METABOLISM (DECREASE USE OF GLUCOSE IN BODY SO INCREASE BLOOD GLUCOSE)

68
Q

LYPOLISIS

A

BREAKDOWN OF FATTY TISSUE

69
Q

WHERE DO THYROID HORMONES ACT TO INCREASE METABOLISM AND PROTEIN SYNTHESIS

A

NEARLY ALL BODY TISSUES

70
Q

WHO NEEDS THYROID HORMONES FOR BRAIN DEVELOPMENT

A

INFANTS
SMALL CHILDREN

71
Q

WHAT IS IODINE NEEDED FOR

A

THE PRODUCTION OF THYROID HORMOMNES

72
Q

WHAT REGULATES THE SECRETION OF THYROID HORMONE

A

HYPOTHALMIC PITUITARY THEYROID SYSTEM

73
Q

2 THYROID HORMONES

A

T4- THYROXINE
T3- TRIIODOTHYRONINE

74
Q

WHAT IS T3 THE ACTIVE FORM OF

A

THYROID HORMONE

75
Q

IN WESTERN CULTURE, WHERE DO WE GET A LOT OF OUR IODINE FROM

A

IODIZED SALT
TABLE SALT
SEAFOOD

76
Q

WHY IS T4 CONVERTED TO T3

A

SO IT CAN PHYSIOLOGICALLY

77
Q

HOW ARE T3 AND T4 STIMULATED

A

TSH

78
Q

THE HYPOTHALAMUS PRODUCES THYROTROPIN RELEASING HORMONE AS A RESULT OF WHAT KIND OF STIMULI

A

IMPROPER SLEEP
COLD TEMP
STRESS

79
Q

WHAT DOES TSH ACT ON

A

DIRECTLY ON THE GLAND ITSELF TO RELEASE T3 AND T4
THIS IS NEGATIVE FEEDBACK

80
Q

ACTIONS OF THE THYROID HORMONE

A

INCREASE METABOLISM AND PROTEIN SYNTHESIS
METABOLIC RATE
CARDIOVASCULAR FUNCTION
GI FUNCTION
NEUROMUSCULAR FUNCTION

81
Q

WHAT DO T3 AND T4 DO FOR THE METABOLIC RATE

A

INCREASE IT IN ALL BODY TISSUES EXCEPT RETINA, SPLEEN, TESTES, AND LUNG

82
Q

WHEN METABOLIC RATE INCREASES, WHAT ELSE INCREASES

A
  1. USE OF GLUCOSE, FAT, PROTEIN
  2. CATABOLISM OF CHOLESTEROL IN LIVER
  3. USE OF VITAMINS
  4. ABSORBTION OF GLUCOSE FROM GI TRACT
83
Q

WHEN METABOLIC RATE INCREASES, WHAT HAPPENS TO LIPIDS

A

METABOLIZED FROM ADIPOSE TISSUES
USED AS FUEL

84
Q

WHEN METABOLIC RATE INCREASES, WHAT HAPPENS TO MUSCLE TISSUES

A

BROKEN DOWN
USED AS FUEL

85
Q

WHAT IN THE CARDIOVASCULAR SYSTEM INCREASES WITH A THYROID HORMONE INCREASE

A

OXYGEN CONSUMPTION
VASODILATION
BLOOD FLOW TO SKIN TO DISSIPATE BODY HEAT GENERATED BY INCREASED METABOLISM
BLOOD VOLUME
CO
VENTILATION
HR
CONTRACTILITY

86
Q

WHAT INCREASES IN THE GI FUNCTION WITH AN INCREASE OF THYROID HORMONE

A

MOTILITY
SECRETION PRODUCTION
APPETITE
FOOD INTAKE
WEIGHT LOSS

87
Q

INCREASE IN THYROID HORMONE CAUSES WHAT NEUROMUSCULAR EFFECTS

A
  1. INCREASED MUSCLE REACTION
  2. NORMAL BRAIN DEVELOPMENT IN THE INFANT
  3. INTERACTION BETWEEN THYROID AND SYMPATHETIC NERVOUS SYSTEM
88
Q

WHAT 3 HORMONES DOES THE ADRENAL CORTEX SECRETE

A

GLUCOCORTICOIDS
MINERALOCORTICOIDS
ADRENAL ANDROGENS

89
Q

THE HYPOTHALMIC PITUITARY ADRENAL SYSTEM REGULATES WHAT

A

RELEASE OF GLUCOCORTICOIDS AND ADRENAL ANDROGENS

90
Q

ADRENAL CORTICAL HORMONES ARE DEACTIVATED BY WHAT

A

THE LIVER AND EXCRETED IN THE URINE OR BILE

91
Q

MINERALOCORTICOIDS

A

FUNCTION IN SODIUM, POTASSIUM, WATER BALANCE
PRIMARY-ALDOSTERONE

92
Q

GLUCOCORTICOIDS

A

FUNCTION IN REGULATION OF METABOLISM, CONTROL INFLAMMATORY/IMMUNE RESPONSE, ESSENTIAL FOR STRESS SURVIVAL
PRIMARY-CORTISOL

93
Q

ADRENAL CORTICAL INSUFFICIENCY

A

MINERALOCORTICOIDS, GLUCOCORTICOIDS DEFICIENCY

94
Q

ADRENAL CORTICAL EXCESS

A

MINERALCORTICOID EXCESS
ANDROGEN EXCESS
GLUCOCORTICOIDS EXCESS

95
Q

HIRSUTISM

A

ANDROGEN EXCESS

96
Q

WITH ADRENAL CORTICALTROPIN RELEASING HORMONES, WHAT ARE EXAMPLES OF STIMULI

A

STRESS
INFECTION
PAIN
HYPOGLYCEMIA
SLEEP
HEMORRHAGE
TRAUMA

97
Q

MINERALCORTICOIDS REGULATE WHAT

A

SODIUM, POTASSIUM, WATER BALANCE

98
Q

PRIMARY MINERALOCORTICOID

A

ALDOSTERONE

99
Q

MINERALCORTICOIDS ARE REGULATED BY

A

RENIN ANGIOTENSIN ALDOSTERONE SYSTEM
RAAS

100
Q

ACTION OF MINERALCORTICOIDS

A

PROMOTE SODIUM, REABSORPTION IN THE DISTAL TUBULES
WATER FOLLOWS SODIUM AND IS EXCRETED IN THE URINE

101
Q

FUNCTION OF GLUCOCORTICOIDS

A

STRESS RESPONSE, CONTROL OF INFLAMMATORY/IMMUNE RESPONSE, REGULATE GLUCOSE, PROTEIN FAT METABOLISM

102
Q

PRIMARY GLUCOCORTICOID

A

CORTISOL

103
Q

GLUCOCORTICOIDS ARE REGULATED BY

A

THE HYPOTHALAMIC PITUITARY ADRENAL SYSTEM

104
Q

WHAT EFFECT DO ADRENAL ANDROGENS HAVE ON SEXUAL FUNCTION

A

LITTLE ON NORMAL SEXUAL FUNCTION

105
Q

PRIMARY ANDROGEN

A

DEHYDROEPIANDROSTERONE
DHEA

106
Q

ADRENAL ANDROGENS CONTRIBUTE TO PUBERTY HOW

A

BODY HAIR GROWTH IN WOMEN

107
Q

WHATA HAPPENS TO ADRENAL ANDROGENS AS WE AGE

A

DECLINE IN PRODUCTION

108
Q

DIABETES INSIPIDUS

A

ADH DISORDER
DEFICIENCY OR DECREASED RESPONSE TO ADH

109
Q

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE

A

ADH DISORDERS
EXCESS ADH SECRETION

110
Q

Where are the releasing hormones released from?

A

THE HYPOTHALAMUS

111
Q

Where are the trophic hormones released from?

A

THE ANTERIOR PITUITARY

112
Q

What two hormones are released from the posterior pituitary

A

adh or vasopressin
oxytocin

113
Q

What is the target organ for TSH?

A

thyroid

114
Q

What is released by the target organ in response to TSH

A

t3 and t4

115
Q

What is the target organ for ACTH?

A

adrenal cortex

116
Q

What is released by the target organ in response to acth

A

cortisol
androgens

117
Q

What is the target organ for FSH and LH?

A

ovarian follicle

118
Q

What hormones are secreted from the posterior pituitary gland?

A

oxytocin and adh aka vasopressin

119
Q

What hormones are secreted from the anterior pituitary gland?

A

tsh
acth
fsh
lh

120
Q

Explain the negative feedback mechanism involved in the regulation of thyroid hormones.

A

The Thyroid Feedback Mechanism. TH regulates TRH gene expression and production through a negative feedback mechanism; TRH expression is high when TH levels are low, and TRH expression is suppressed when TH levels are increased.

121
Q

What is the physiologic effect of insulin?

A

carb metabolism
increases rate of transport of glucose across the cell membrane in adipose tissue and muscle
increases rate of glycolysis
stimulates the rate of glycogen synthesis

122
Q

What is the physiologic effect of glucagon?

A

Glucagon is secreted into the portal vein and thus has its major physiologic action at the liver to break down glycogen.

123
Q

What happens to glucose when the liver and skeletal muscle tissue are saturated and can no longer store glycogen?

A

the “excess” glucose is “converted” to fat tissue through catabolism IN the fat cells, which essentially “grow” with the glucose consumed… and, by the way… this process actually burns off some of the glucose… about 10% of the amount stored is “burned” to store it.

124
Q

What clinical manifestations would be observed in a child with GH deficiency?

A

slow height growth each year after a child’s 3rd birthday. A child with GH deficiency may also have a younger-looking face and a chubby body build.

125
Q

What is the pathophysiology for Diabetes Insipidus (DI)?

A

when your body doesn’t make enough antidiuretic hormone (ADH) or your kidneys don’t use it properly. Your body needs ADH to retain appropriate amounts of water. Without ADH, your body loses water through urine. Diabetes mellitus is much more common than diabetes insipidus

126
Q

What is the pathophysiologic difference between type I and type II diabetes mellitus?

A

In diabetes type 1, the pancreas does not make insulin, because the body’s immune system attacks the islet cells in the pancreas that make insulin. In diabetes type 2, the pancreas makes less insulin than used to, and your body becomes resistant to insulin.

127
Q

What electrolyte imbalances should the nurse suspect in Addison’s disease?

A

hyponatremia, hyperkalemia, and hypoglycemia.

128
Q

What are the clinical manifestations of hypoglycemia?

A

Fast heartbeat.
Shaking.
Sweating.
Nervousness or anxiety.
Irritability or confusion.
Dizziness.
Hunger.

129
Q

What clinical manifestations may be seen in a client with Cushing’s Syndrome?

A

their face get round (“moon face”), they gain weight in unusual ways, bruise easily or feel weak, tired and sad.

130
Q

What electrolyte is involved in excitatory amino acid injury?

A

acid glutamate

131
Q

What is the difference between brain death and a persistent vegetative state?

A

A persistent vegetative state means the person has lost higher brain functions, but their undamaged brain stem still allows essential functions like heart rate and respiration to continue. A person in a vegetative state is alive and may recover to some degree, given time. Brain death means the person has died.

132
Q

Describe where production and flow of CSF occurs. What occurs when there is excess of CSF?

A

Hydrocephalus is a buildup of cerebrospinal fluid (CSF) in the spaces deep inside your brain (ventricles). As a result of the excess fluid, the ventricles widen and put pressure on the brain tissue. In hydrocephalus, the cycle that allows CSF fluid to flow freely is out of balance and fluid builds up in the ventricles.

133
Q

Order the meningeal layers of the brain starting from the outermost to innermost layer

A

dura mater
arachnoid
pia mater

134
Q

Interpret the Glasgow Coma Scale—what does it mean when the client’s GCS is increasing?Decreasing

A

Based on the level of consciousness, a score is assigned. A higher score indicates a greater level of consciousness. The GCS uses three sites for stimulation. This includes fingertip pressure, trapezius pinch and supraorbital notch.

135
Q

What cranial nerve is responsible for pupillary changes?

A

oculomotor nerve
cn iii

136
Q

what is the formula for cpp

A

cpp = map - icp

137
Q

what is normal icp

A

7-15 mmhg

138
Q

what is normal cpp

A

60-80 mmhg

139
Q

What are the 3 major causes/classifications of increased ICP

A

brain, cerebrospinal fluid, and blood. Any increase in the volume of its contents will increase the pressure within the cranial vault. An increase in the volume of one component will result in a decrease in volume in one or two of the other components.

140
Q

Monroe-Kellie Hypothesis

A

What finally came to be known as the Monro-Kellie doctrine, or hypothesis, is that the sum of volumes of brain, CSF, and intracranial blood is constant. An increase in one should cause a decrease in one or both of the remaining two.

141
Q

What is the difference between a stroke and a TIA?

A

A TIA is a brief blockage of blood flow to part of the brain, spinal cord or the thin layer of tissue at the back of the eye known as the retina. This blockage may cause temporary stroke-like symptoms. But a TIA doesn’t damage brain cells or cause permanent disability. This is how it differs from a regular stroke.

142
Q

What vessel is commonly damaged in patients with epidural hematoma?

A

middle meningeal artery

143
Q

What acronym do we use to assess for s/s of stroke?

A

be fast
balance
eyes
face
arm
speech
time

144
Q

What is the target organ for FSH and LH?

A

anterior pituitary

145
Q

A __________ (primary, secondary,tertiary) disorder is associated with damage to the hypothalamus

A

tertiary

146
Q

A tumor that causes damage to the thyroid gland is an example of a____________ (primary, secondary, tertiary) disorder.

A

primary

147
Q

A tumor that destroys the posterior pituitary gland is an example of a____________(primary, secondary, tertiary) disorder?

A

secondary

148
Q

what stimulates the production of gh

A

ghrh

149
Q

gh

A

somadotropin

150
Q

what inhibits the production of gh

A

somadastatin
ghih

151
Q

ghrh and ghih are released from

A

hypothalamus

152
Q

growth hormone
igf 1 deficiency

A
  • Idiopathic GH deficiency- Lacks hypothalamic
    GHRH
  • Pituitary tumors, agenesis of the pituitary- Cannot produce GH
  • Laron-type dwarfism- Hereditary defect in IGF production
153
Q

growth hormone
igf1
excess

A
  • Gigantism - childhood* Before puberty and fusion of epiphyseal plates
  • Acromegaly – adult* After fusion of epiphyseal plates
154
Q

gh excess in adults

A

Overgrowth of the small bones and cartilaginous parts of the skeleton
* Epiphyseal plates closed –don’t grow taller
* Enlargement of the heart and other organs of the body
* Metabolic disturbances resulting in altered fat metabolism and impaired glucose tolerance - can lead to diabetes

155
Q
A

312 Patho (3 decks)

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