PATHO FINAL Flashcards
(155 cards)
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
2
Q
HORMONES
A
CHEMICAL MESSENGERS
3
Q
WHAT DOES THE ENDOCRINE SYSTEM OVERLAP WITH
A
NERVOUS SYSTEM AND IMMUNE SYSTEM
*TERMS LIKE NEUROENDOCRINE IMMUNE SYSTEM
4
Q
WHAT DOES THE ENDOCRINE SYSTEM DO
A
- GROWTH AND DEVELOPMENT
- SEX DIFFERENTIATION- REPRODUCTION
- METABOLISM-DIGESTION, USE AND STORAGE OF NUTRIENTS, REGULATION OF SOME ELECTROLYTES AND FLUIDS
- ADAPTATION TO AN EVERY CHANGING ENVIRONMENT- HOMEOSTASIS
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
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
7
Q
RECEPTORS ON CELL (SURFACE OR INTRACELLULAR) REACT
A
TO HORMONE TO PRODUCE EFFECT
8
Q
WHERE ARE HORMONES RELEASED
A
ENDOCRINE GLANDS
1. PITUITARY GLAND
2. THYROID GLAND
3. ADRENAL GLAND
4. PANCREAS
9
Q
CLASSES OF HORMONES
A
AMINES
AMINO ACIDS
PEPTIDES
POLYPEPTIDES
PROTEINS
STEROIDS
FATTY ACIDS
10
Q
PARACRINE HORMONES
A
ACT LOCALLY
DO NOT ENTER THE BLOOD STREAM
EX: SEX HORMONES ON THE OVARY
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
12
Q
RELEASING HORMONES FROM THE HYPOTHALAMUS DO WHAT
A
TELL THE PITUITARY WHAT TO RELEASE INTO THE BLOOD
13
Q
BESIDES RELEASING HORMONES, WHAT ELSE CAN THE HYPOTHALAMUS RELEASE
A
PITUITARY INHIBITING HORMONES
14
Q
HORMONES FROM THE PITUITARY TELL SPECIFIC PERIPHERAL GLANDS TO WHAT
A
GROW AND PRODUCE THEIR HORMONES
15
Q
HYPOTHALAMUS-PITUITARY-TARGET CELL SYSTEM
A
HYPOTHALAMUS –> RELEASING HORMONES OR PITUITARY INHIBITING HORMONES –> TELL PERIPHERAL GLANDS TO PRODUCE HORMONES
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
17
Q
EXAMPLES OF HORMONES WITH 24 HR FLUCTUATION
A
THOSE THAT REGULATE OUR SLEEP/WAKE CYCLE
18
Q
EXAMPLES OF HORMONES WITH A 28 DAY PERIOD
A
MENTAL CYCLE
19
Q
HOW IS HORMONE SECRETION MOST OFTEN REGULATED
A
NEGATIVE FEEDBACK THAT MONITOR SUBSTANCES AND STIMULI IN THE BODY TO PRODUCE A RESPONSE
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
21
Q
WHAT DO TROPIC HORMONES DO
A
STIMULATE OR INHIBIT THE TARGET GLAND THEY ARE LOOKING AT
22
Q
HOW IS THE PITUITARY GLAND DIVIDED
A
ANTERIOR AND POSTERIOR
23
Q
WHAT DOES THE ANTERIOR PITUITARY RELEASE
A
ADH
OXYTOCIN
24
Q
WHAT DOES THE POSTERIOR PITUITARY GLAND RELEASE
A
GROWTH HORMONES
TSH
ADRENOCORTICOTROPIC HORMONE
FOLLICLE STIMULATING HORMONE
LUTENIZING HORMONE
PROLACTIN
25
FEEDBACK REGULATION
SENSORS IN THE BODY DETECT A CHANGE AND ADJUST HORMONE SECRETION TO MAINTAIN BLOOD LEVELS
26
NEGATIVE FEEDBACK
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
27
EXAMPLE OF NEGATIVE FEEDBACK SYSTEM
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
28
POSITIVE FEEDBACK SYSTEM
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
29
EXAMPLE OF POSITIVE FEEDBACK
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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ALTERED ENDOCRINE FUNCTION
HYPOFUNCTION
HYPERFUNCTION
HORMONE RECEPTOR RESISTANCE
31
ENDOCRINE HYPOFUNCTION
CONGENITAL DEFECTS
GLAND DESTRUCTION
32
CONGENITAL DEFECTS
ABSENCE OF OR IMPAIRED FUNCTION
ABSENCE OF ENZYME NEEDED TO MAKE HORMONES
33
GLAND DESTRUCTION
DECREASED BLOOD FLOW, INFECTION, INFLAMMATION, AUTOIMMUNE RESPONSES, TUMORS
34
HORMONE RECEPTOR RESISTANCE
ABSENCE OF RECEPTORS
DEFECT IN RECEPTOR BINDING
35
ENDOCRINE HYPERFUNCTION
EXCESSIVE STIMULATION AND HYPERPLASIA OF THE GLAND
HORMONE PRODUCING TUMOR
ADMIN OF EXOGENOUS HORMONES
36
HOW ARE ENDOCRINE DISORDERS CLASSIFIED
PRIMARY
SECONDARY
TERTIARY
*DEPENDING ON LOCATION OF DYSFUNCTION IN THE HPT ORGAN SYSTEM
37
TERTIARY
DYSFUNCTION IN STIMULATION FROM THE HYPOTHALAMUS
38
SECONDARY
DYSFUNCTION IN STIMULATION FROM THE PITUITARY
39
PRIMARY
DYSFUNCTION IN THE TARGET ORGAN/GLAND
40
WHAT HORMONES GENERALLY COME FROM THE HYPOTHALAMUS
RELEASING HORMONES, BUT SOME HAVE INHIBITORY PROPERTIES
41
WHAT IS THE PRIMARY JOB OF THE HORMONES COMING FROM THE HYPOTHALAMUS
STIMULATE THE PITUITARY TO RELEASE TROPIC HORMONES
42
GHRH
GROWTH HORMONE RELEASING HORMONE
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TRH
THYROTROPIN RELEASING HORMONE
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CRH
CORTICOTROPIN RELEASING HORMONE
AIDS IN RELEASE OF HORMONES FROM ADRENAL CORTEX
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GRH
GONADOTROPIN RELEASING HORMONE
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HYPOTHALAMIC HORMONES
GHRH
TRH
CRH
GRH
SOMATOSTATIN
DOPAMINE
47
SOMATOSTATIN
INHIBITORY HORMONE
INHIBITS GHRH AND TSH
DELAYS INTESTINAL ABSORPTION OF GLUCOSE
48
DOPAMINE
INHIBITORY HORMONE
INHIBITS PROLACTIN, FSH, LUTEINIZING HORMONE
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POTERIOR PITUITARY HORMONES
ADH
OXYTOCIN
50
ADH
INCREASE REABSORPTION OF WATER AND SODIUM BY THE KIDNEY THUS INCREASING OUR VASCULAR VOLUME AND OUR OXYTOCIN
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OXYTOCIN
STIMULATES UTERINE CONTRACTIONS IN PREGNANT WOMEN
MILK PRODUCTION AFTER CHILDBIRTH
52
ANTERIOR PITUITARY HORMONES
GH
FSH
LH
TSH
ACTH
53
GH
GROWTH HORMONE
STIMULATE GROWTH OF BONE AND MUSCLE
PROMOTES PROTEIN SYNTHESIS AND FAT METABOLISM
DECREASES CARB METABOLISM
54
FSH
FOLLICLE STIMULATING HORMONE
STIMULATES THE GROWTH OF THE OVARIAN FOLLICLE AS WELL AS OVULATION
IN MEN, IT STIMULLATES SPERM PRODUCTION
55
LH
LUTEINIZING HORMONE
WOMEN-STIMULATE OOCYTE, PRODUCTION OF ESTROGEN, AND PROGESTERONE
MEN- DEVELOPMENT OF TESTI TISSUE, STIMULATE SECRETION OF TESTOSTERONE
56
TSH
THYROID STIMULATING HORMONE
STIMULATES THE SYNTHESIS AND SECRETION OF OUR THYROID HORMONES
57
ACTH
ADRENOCORTICOTROPHIC HORMONE
STIMULATES THE SYNTHESIS AND SECRETION OF OUR ADRENAL CORTICAL HORMONES
58
GH SECRETION IS STIMULATED BY
HYPOGLYCEMIA
FASTING
STARVATION
STRESS
59
GH INHIBITED BY
INCREASED GLUCOSE
FREE FATTY ACID RELEASE
OBESITY
CORTISOL
60
GH IS ALSO KNOWN AS
SOMADOTROPIN
61
WHAT DOES GH DO
LATERAL BONE GROWTH
METABOLISM
CARTILAGE GROWTH
62
WHAT IS THE GROWTH HORMONE RELEASING HORMONE
GHRH
63
WHAT IS OUR GH INHIBITING HORMONE
SOMATOSTATIN
64
ACTS OF GROWTH HORMONE
GROWTH PROMOTING ACTIONS
ANTI-INSULINE EFFECTS
*ACTS ON THE LIVER
DOESN'T DIRECTLY CAUSE BONE GROWTH
65
WHAT DOES THE LIVER PRODUCE FOR BONE GROWTH WHEN STIMULATED BY GH
IGF
66
IGF
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
ANTI-INSULIN EFFECTS OF GH
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)
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LYPOLISIS
BREAKDOWN OF FATTY TISSUE
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WHERE DO THYROID HORMONES ACT TO INCREASE METABOLISM AND PROTEIN SYNTHESIS
NEARLY ALL BODY TISSUES
70
WHO NEEDS THYROID HORMONES FOR BRAIN DEVELOPMENT
INFANTS
SMALL CHILDREN
71
WHAT IS IODINE NEEDED FOR
THE PRODUCTION OF THYROID HORMOMNES
72
WHAT REGULATES THE SECRETION OF THYROID HORMONE
HYPOTHALMIC PITUITARY THEYROID SYSTEM
73
2 THYROID HORMONES
T4- THYROXINE
T3- TRIIODOTHYRONINE
74
WHAT IS T3 THE ACTIVE FORM OF
THYROID HORMONE
75
IN WESTERN CULTURE, WHERE DO WE GET A LOT OF OUR IODINE FROM
IODIZED SALT
TABLE SALT
SEAFOOD
76
WHY IS T4 CONVERTED TO T3
SO IT CAN PHYSIOLOGICALLY
77
HOW ARE T3 AND T4 STIMULATED
TSH
78
THE HYPOTHALAMUS PRODUCES THYROTROPIN RELEASING HORMONE AS A RESULT OF WHAT KIND OF STIMULI
IMPROPER SLEEP
COLD TEMP
STRESS
79
WHAT DOES TSH ACT ON
DIRECTLY ON THE GLAND ITSELF TO RELEASE T3 AND T4
THIS IS NEGATIVE FEEDBACK
80
ACTIONS OF THE THYROID HORMONE
INCREASE METABOLISM AND PROTEIN SYNTHESIS
METABOLIC RATE
CARDIOVASCULAR FUNCTION
GI FUNCTION
NEUROMUSCULAR FUNCTION
81
WHAT DO T3 AND T4 DO FOR THE METABOLIC RATE
INCREASE IT IN ALL BODY TISSUES EXCEPT RETINA, SPLEEN, TESTES, AND LUNG
82
WHEN METABOLIC RATE INCREASES, WHAT ELSE INCREASES
1. USE OF GLUCOSE, FAT, PROTEIN
2. CATABOLISM OF CHOLESTEROL IN LIVER
3. USE OF VITAMINS
4. ABSORBTION OF GLUCOSE FROM GI TRACT
83
WHEN METABOLIC RATE INCREASES, WHAT HAPPENS TO LIPIDS
METABOLIZED FROM ADIPOSE TISSUES
USED AS FUEL
84
WHEN METABOLIC RATE INCREASES, WHAT HAPPENS TO MUSCLE TISSUES
BROKEN DOWN
USED AS FUEL
85
WHAT IN THE CARDIOVASCULAR SYSTEM INCREASES WITH A THYROID HORMONE INCREASE
OXYGEN CONSUMPTION
VASODILATION
BLOOD FLOW TO SKIN TO DISSIPATE BODY HEAT GENERATED BY INCREASED METABOLISM
BLOOD VOLUME
CO
VENTILATION
HR
CONTRACTILITY
86
WHAT INCREASES IN THE GI FUNCTION WITH AN INCREASE OF THYROID HORMONE
MOTILITY
SECRETION PRODUCTION
APPETITE
FOOD INTAKE
WEIGHT LOSS
87
INCREASE IN THYROID HORMONE CAUSES WHAT NEUROMUSCULAR EFFECTS
1. INCREASED MUSCLE REACTION
2. NORMAL BRAIN DEVELOPMENT IN THE INFANT
3. INTERACTION BETWEEN THYROID AND SYMPATHETIC NERVOUS SYSTEM
88
WHAT 3 HORMONES DOES THE ADRENAL CORTEX SECRETE
GLUCOCORTICOIDS
MINERALOCORTICOIDS
ADRENAL ANDROGENS
89
THE HYPOTHALMIC PITUITARY ADRENAL SYSTEM REGULATES WHAT
RELEASE OF GLUCOCORTICOIDS AND ADRENAL ANDROGENS
90
ADRENAL CORTICAL HORMONES ARE DEACTIVATED BY WHAT
THE LIVER AND EXCRETED IN THE URINE OR BILE
91
MINERALOCORTICOIDS
FUNCTION IN SODIUM, POTASSIUM, WATER BALANCE
PRIMARY-ALDOSTERONE
92
GLUCOCORTICOIDS
FUNCTION IN REGULATION OF METABOLISM, CONTROL INFLAMMATORY/IMMUNE RESPONSE, ESSENTIAL FOR STRESS SURVIVAL
PRIMARY-CORTISOL
93
ADRENAL CORTICAL INSUFFICIENCY
MINERALOCORTICOIDS, GLUCOCORTICOIDS DEFICIENCY
94
ADRENAL CORTICAL EXCESS
MINERALCORTICOID EXCESS
ANDROGEN EXCESS
GLUCOCORTICOIDS EXCESS
95
HIRSUTISM
ANDROGEN EXCESS
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WITH ADRENAL CORTICALTROPIN RELEASING HORMONES, WHAT ARE EXAMPLES OF STIMULI
STRESS
INFECTION
PAIN
HYPOGLYCEMIA
SLEEP
HEMORRHAGE
TRAUMA
97
MINERALCORTICOIDS REGULATE WHAT
SODIUM, POTASSIUM, WATER BALANCE
98
PRIMARY MINERALOCORTICOID
ALDOSTERONE
99
MINERALCORTICOIDS ARE REGULATED BY
RENIN ANGIOTENSIN ALDOSTERONE SYSTEM
RAAS
100
ACTION OF MINERALCORTICOIDS
PROMOTE SODIUM, REABSORPTION IN THE DISTAL TUBULES
WATER FOLLOWS SODIUM AND IS EXCRETED IN THE URINE
101
FUNCTION OF GLUCOCORTICOIDS
STRESS RESPONSE, CONTROL OF INFLAMMATORY/IMMUNE RESPONSE, REGULATE GLUCOSE, PROTEIN FAT METABOLISM
102
PRIMARY GLUCOCORTICOID
CORTISOL
103
GLUCOCORTICOIDS ARE REGULATED BY
THE HYPOTHALAMIC PITUITARY ADRENAL SYSTEM
104
WHAT EFFECT DO ADRENAL ANDROGENS HAVE ON SEXUAL FUNCTION
LITTLE ON NORMAL SEXUAL FUNCTION
105
PRIMARY ANDROGEN
DEHYDROEPIANDROSTERONE
DHEA
106
ADRENAL ANDROGENS CONTRIBUTE TO PUBERTY HOW
BODY HAIR GROWTH IN WOMEN
107
WHATA HAPPENS TO ADRENAL ANDROGENS AS WE AGE
DECLINE IN PRODUCTION
108
DIABETES INSIPIDUS
ADH DISORDER
DEFICIENCY OR DECREASED RESPONSE TO ADH
109
SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE
ADH DISORDERS
EXCESS ADH SECRETION
110
Where are the releasing hormones released from?
THE HYPOTHALAMUS
111
Where are the trophic hormones released from?
THE ANTERIOR PITUITARY
112
What two hormones are released from the posterior pituitary
adh or vasopressin
oxytocin
113
What is the target organ for TSH?
thyroid
114
What is released by the target organ in response to TSH
t3 and t4
115
What is the target organ for ACTH?
adrenal cortex
116
What is released by the target organ in response to acth
cortisol
androgens
117
What is the target organ for FSH and LH?
ovarian follicle
118
What hormones are secreted from the posterior pituitary gland?
oxytocin and adh aka vasopressin
119
What hormones are secreted from the anterior pituitary gland?
tsh
acth
fsh
lh
120
Explain the negative feedback mechanism involved in the regulation of thyroid hormones.
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
What is the physiologic effect of insulin?
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
What is the physiologic effect of glucagon?
Glucagon is secreted into the portal vein and thus has its major physiologic action at the liver to break down glycogen.
123
What happens to glucose when the liver and skeletal muscle tissue are saturated and can no longer store glycogen?
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
What clinical manifestations would be observed in a child with GH deficiency?
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
What is the pathophysiology for Diabetes Insipidus (DI)?
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
What is the pathophysiologic difference between type I and type II diabetes mellitus?
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
What electrolyte imbalances should the nurse suspect in Addison’s disease?
hyponatremia, hyperkalemia, and hypoglycemia.
128
What are the clinical manifestations of hypoglycemia?
Fast heartbeat.
Shaking.
Sweating.
Nervousness or anxiety.
Irritability or confusion.
Dizziness.
Hunger.
129
What clinical manifestations may be seen in a client with Cushing’s Syndrome?
their face get round ("moon face"), they gain weight in unusual ways, bruise easily or feel weak, tired and sad.
130
What electrolyte is involved in excitatory amino acid injury?
acid glutamate
131
What is the difference between brain death and a persistent vegetative state?
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
Describe where production and flow of CSF occurs. What occurs when there is excess of CSF?
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
Order the meningeal layers of the brain starting from the outermost to innermost layer
dura mater
arachnoid
pia mater
134
Interpret the Glasgow Coma Scale—what does it mean when the client’s GCS is increasing?Decreasing
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
What cranial nerve is responsible for pupillary changes?
oculomotor nerve
cn iii
136
what is the formula for cpp
cpp = map - icp
137
what is normal icp
7-15 mmhg
138
what is normal cpp
60-80 mmhg
139
What are the 3 major causes/classifications of increased ICP
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
Monroe-Kellie Hypothesis
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
What is the difference between a stroke and a TIA?
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
What vessel is commonly damaged in patients with epidural hematoma?
middle meningeal artery
143
What acronym do we use to assess for s/s of stroke?
be fast
balance
eyes
face
arm
speech
time
144
What is the target organ for FSH and LH?
anterior pituitary
145
A __________ (primary, secondary,tertiary) disorder is associated with damage to the hypothalamus
tertiary
146
A tumor that causes damage to the thyroid gland is an example of a____________ (primary, secondary, tertiary) disorder.
primary
147
A tumor that destroys the posterior pituitary gland is an example of a____________(primary, secondary, tertiary) disorder?
secondary
148
what stimulates the production of gh
ghrh
149
gh
somadotropin
150
what inhibits the production of gh
somadastatin
ghih
151
ghrh and ghih are released from
hypothalamus
152
growth hormone
igf 1 deficiency
* Idiopathic GH deficiency- Lacks hypothalamic
GHRH
* Pituitary tumors, agenesis of the pituitary- Cannot produce GH
* Laron-type dwarfism- Hereditary defect in IGF production
153
growth hormone
igf1
excess
* Gigantism - childhood* Before puberty and fusion of epiphyseal plates
* Acromegaly – adult* After fusion of epiphyseal plates
154
gh excess in adults
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
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