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Pathophysiology > Unit 12 > Flashcards

Unit 12 Flashcards

1
Q

hormone mechanisms can be amplified and spread throughout the cell by

A

second messengers

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2
Q

diverse structure of hormones

A

amines and amino acids
peptides
proteins
steroids
fatty acid

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3
Q

different hormones have different

A

half lives

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4
Q

what are the different ways a hormone can be destroyed

A

enzymes, by the cell, by the liver

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5
Q

2 types of hormone receptor interactions

A

surface (second messenger) and intracellular interactions

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6
Q

examples of surface hormone receptor interactions

A

cAMP, glucagon, insulin, epinephrine, pth, TSH, ACTH, FSH, LH, ADH

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7
Q

up regulation

A

cells make more receptors

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8
Q

down regulation

A

cells make fewer receptors

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9
Q

response of a hormone depends on the receptor number and

A

affinity

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10
Q

your patient has low levels of circulating thyroid hormone. how will the cells of the thyroid gland respond

A

up regulation

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11
Q

aniterior pituitary

A

gland

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12
Q

posterior pituitary

A

neural

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13
Q

hypothalamus detects the state of the bodys

A

temp
blood osmolarity
blood nutrients
blood hormones
inflammatory mediatiors
emotions
pain

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14
Q

T/F: the pituitary gland controls the release of thyroid hormone

A

T

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15
Q

the pituitary gland tells other organs/glands to produce and secrete or inhibit the appropriate hormones. Where does the pituitary glad receive the cue to act from

A

hypothalamus

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16
Q

hypofunction

A

underproduction

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17
Q

causes of hypofunction

A

decline with aging
atrophy
congenital defects
disruption in blood flow
infection
inflammation
autoimmune responses
neoplastic growth
receptor defects

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18
Q

hyperfunction

A

excessive hormone production

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19
Q

causes of hyperfunction

A

excessive stimulation and hyperplasia of the endocrine gland
hormone producing tumor of the gland (PARENOPLASTIC)

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20
Q

primary disorders

A

originate in the target gland

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21
Q

secondary disorders

A

target gland is normal but its function is altered by defective levels of stimulating hormones or releasing factors from the pituitary system

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22
Q

tertiary disorders

A

result from hypothalamic dysfunction
both pituitary and target organ are under stimulated

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23
Q

T4 is inactive until converted into __ in tissues

A

T3

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24
Q

both thyroid hormones exert a

A

negative feedback

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25
Q

thyroid hormone increases metabolism and ________ synthesis

A

protein

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26
Q

if there is thyroid deficit in infancy this may cause

A

mental retardation

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27
Q

thyroid has strong interactions with

A

SNS and ANS

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28
Q

if you suspect you might have a thyroid issue what is the first test that would be done

A

blood sample

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29
Q

HYPOthyroid BMR is

A

decreased

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30
Q

HYPOthyroid will have ___________ sensitivity to catecholamines

A

decreased

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31
Q

HYPOthyroid will have ______________ features

A

myxedematous

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32
Q

HYPOthyroid will make people feel

A

sluggish

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33
Q

HYPOthyroid ____________ CO

A

decrease

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34
Q

HYPOthyroid _______cardia

A

brady

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35
Q

HYPOthyroid will have ________ with their bowel movements

A

constipation

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36
Q

HYPOthyroid will have ______ventilation

A

hypo

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37
Q

HYPOthyroid will be _____ intolerant

A

cold

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38
Q

HYPOthyroid will have weight

A

gain

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39
Q

HYPOthyroid will have coarse ____ skin and hair

A

dry

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40
Q

HYPOthyroid will have ________ muscle tone

A

decreased

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41
Q

HYPERthyroid will have BMR

A

increased

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42
Q

HYPERthyroid will have ________ sensitivity to catecholamines

A

increased

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43
Q

HYPERthyroid will appear with exophthalmus which is what

A

bulging eyes that look like a pug

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44
Q

HYPERthyroid will make the patient feel

A

restlessness, irritability, anxiety

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45
Q

HYPERthyroid will have _________ CO

A

increased

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46
Q

HYPERthyroid will have _______cardia

A

tachy

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47
Q

HYPERthyroid will have what kind of bowel movements

A

diarrhea

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48
Q

HYPERthyroid will have what kind of breathing

A

dyspena

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49
Q

HYPERthyroid will be _______ intolerant

A

heat

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50
Q

HYPERthyroid will have weight ________

A

loss

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51
Q

HYPERthyroid will have thin and ______ hair and skin

A

silky

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52
Q

HYPERthyroid will also have the patient

A

tremor and twitching

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53
Q

if there is a lack of iodine the T3 and T4 will

A

not be made

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54
Q

the lack of iodine will cause no negative feedback there for

A

TRH and TSH will continue to be made

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55
Q

when there is a lack of iodine the patient may present with a

A

goiter

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56
Q

you need what to make T3 and T4

A

iodine

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57
Q

hypothyroidism can be

A

congenital or acquired

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58
Q

an example of acquired hypothyroidism besides the thyroidectomy is

A

Hashimoto thyroiditis

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59
Q

Hashimoto thyroiditis is

A

autoimmune

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60
Q

2 types of hyperthyroidism

A

graves and thyroid tumors

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61
Q

graves is

A

hyperthyroidism

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62
Q

a person with graves disease may physically present how?

A

with wasting, goiter, opthalmopathy (esothalamus)

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63
Q

graves disease is most common in

A

women

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64
Q

graves is an

A

autoimmune disorder

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65
Q

graves disease will have an abnormal stimulation of thyroid gland by

A

thyroid stimulating antibodies

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66
Q

in graves disease exophthalmos results when

A

antibodies interact with antigens found in fibroblasts in orbital tissue behind the eyeball

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67
Q

thyroid storm is a life threating form of

A

thyrotoxicosis

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68
Q

thyroid storm can be causes by

A

stress, infection, DKA, trauma

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69
Q

thyroid storm is manifested by

A

very high fever, tachycardia, CHF, angina and exaggeration CNS symptoms

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70
Q

can you treat thyroid storms with out urgency

A

NO must treat with urgency, life threatening

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71
Q

T/F: goiters are always associated with increased production of thyroid hormone

A

F, can occur with hypo, hyper and euthyroid

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72
Q

euthyroid is

A

when the thyroid is functioning normally

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73
Q

adrenal medulla secretes

A

epi and norepi

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74
Q

the adrenal cortex is responsible for

A

life essential hormones

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75
Q

cortex secretes

A

glucocorticoids, mineralocoricoids, adrenal sex hormones

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76
Q

mineralocoricoid example

A

aldosterone

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77
Q

mineralocoricoid function in balance of what 3 things

A

sodium, potassium, water

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78
Q

adrenal sex hormones example

A

androgens

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79
Q

glucocorticoids example

A

cortisol

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80
Q

glucocorticoids are essential for survival in

A

stress

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81
Q

glucocorticoids regulates metabolic functions of body and controlling

A

inflammatory resposne

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82
Q

actions of cortisol

A

plasma proteins increased, immune/inflammatory systems suppressed, muscle breakdown, free fatty acids increased, SNS response increased, blood glucose increased

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83
Q

cortisol release can be impacted when

A

there is a disease, stress or use of pretinzones

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84
Q

glucocorticoids diurnal variation peak in

A

early morning

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85
Q

glucose metabolism stimulates __________ and __________ glucose use which causes ________ in glucose

A

gluconeogenesis, decreased, increase

86
Q

many people do not like to take glucocorticoids because of

A

psychological effect

87
Q

long term therapy with pharmacolgoic preparations of the adrenal cortical hormone may casue

A

adrenal insufficiency on withdrawl

88
Q

when on glucocorticoids for extended periods of time the adrenals

A

atrophy

89
Q

if you have been talking glucocorticoids for extended periods of time and stop abruptly will you or will you not have any adrenal function

A

you will not, recovery might take 12 months

90
Q

a primary diease of adrenal insufficiency is

A

Addisons disease

91
Q

Addisons disease is caused by

A

destruction of gland

92
Q

Addisons disease is

A

rare autoimmune

93
Q

Addisons disease does not manifest until ___% is destroyed

A

90

94
Q

adrenal insufficiency secondary results from a disorder of

A

HPA system

95
Q

glucocorticoid hormone excess

A

cushings syndrome

96
Q

cushings syndrome can be caused by

A

parenoplastic tumor, long term therapy

97
Q

cushings syndrome apperances

A

buffalo hump, moon face, protruding abdomen, purple striae, muscle wasting, osteoporosis, 20% become DM, hypokalemia, hypertension, inhibited immune response

98
Q

HPA system is the

A

target of steriods

99
Q

Addisons disease will present with

A

bronzy tan hyperpigmentation, hypoglycemia, loss of weight, hypotension, adrenal atrophy, urinary losses, retention of potassium

100
Q

types of cushings syndrome

A

Cushing diease, ectopic cushings syndrome, iatrogenic Cushing syndrome

101
Q

Diabetes Mellitus is a disorder of ______, ______, and _____ metabolism resulting from a lack of insulin availability or a reduction in the biological effects of insulin

A

carb, protein, fat

102
Q

what is the new tool to diagnose DM earlier

A

A1C

103
Q

normal A1C is

A

4-6%

104
Q

type 2 diabetes mainly affects

A

white people non hispanic

105
Q

why would someone have a higher risk for type 2 diabetes

A

overweight/obesity, 45 and older, first gen relative with type 2 diabetes, physically active less than 3 times a week, had gestational diabetes, gave birth to a big baby, or certain race

106
Q

alpha cells released

A

glucagon

107
Q

beta cells release

A

insulin and amylin

108
Q

glucagon

A

causes cells to release stored food into the blood

109
Q

insulin

A

allows cells to take up glucose from the blood

110
Q

ways to test for DM

A

fasting plasma glucose test
random glucose test
oral glucose tolerance test
capillary whole blood glucose monitoring
hemoglobin A1C

111
Q

increased blood glucose causes

A

insulin secretion

112
Q

insulin stimulates uptake, use, and storage of

A

glucose

113
Q

glucose to glycogen

A

glycogenesis

114
Q

glucose to fat

A

lipogenesis

115
Q

insulin inhibits

A

glycogen breakdown
fat breakdown
protein breakdown

116
Q

glycogen breakdown

A

glycogenolysis

117
Q

fat breakdown

A

lipolysis

118
Q

protein breakdown into glucose

A

gluconeogenesis

119
Q

if someone lacks insulin what happens to their blood glucose levels

A

increase

120
Q

if someone lacks insulin what happens to their blood pH

A

decreases, become acidosis

121
Q

liver regulates blood glucose through 3 processes

A

glycogenesis, glycogenolysis, gluconeogenesis

122
Q

synthesis of glucose from non carb souces

A

gluconeogenesis

123
Q

glucose levels rise

A

removed form blood and converted to glycogen

124
Q

glucose levels fall

A

liver glycogen stores broken down and release into circulation

125
Q

liver only uses a small amount of fatty acids for its own energy needs; converts the retainer into

A

ketones and is released into the blood

126
Q

ketones

A

organic acids that cause ketoacidosis when they are present in excessive ammounts

127
Q

when someone has severe metabolic acidosis you will have an increase in __ ____ into the cell which causes __ to leave the cell

A

H ion, K+

128
Q

K+ is the main ____________ ion

A

INTRACELLULAR

129
Q

ketoacidosis causes an increase in K+ how do you fix this

A

fix the acidosis and the K+ will fix it self

130
Q

insulin lowers glucose by

A

facilitating movement of glucose into body tissues

131
Q

actions of insulin include

A

promotes glucose uptake by target cells, glucose breakdown, inhibits gluconeogenesis, increases protein synthesis

132
Q

decreased blood glucose leads to

A

glucagon secretion

133
Q

glucagon stimulates release of glucose into

A

blood

134
Q

glycogen into glucose

A

glycogenolysis

135
Q

fat into fatty acids for energy

A

lipolysis

136
Q

amino acids into glucose

A

gluconeogenesis

137
Q

glucagon maintains blood glucose by increasing the release of

A

glucose from the liver into the blood

138
Q

glucocorticoids stimulate ______________ 6-10 fold increase

A

gluconeogenesis

139
Q

type 1A

A

autoimmune destruction of pancreatic beta cells

140
Q

type 1B

A

idiopathic diabetes

141
Q

type 2

A

beta cell dysfunction and insulin resistance, increased hepatic production of glucose

142
Q

T/F: DM 2 is more common than DM 1

A

true

143
Q

in type 1 diabetes with the absence of insulin

A

free fatty acids are released from fat cells and converted to ketoacids in the liver

144
Q

what type is more prone to DKA

A

type 1

145
Q

all type 1A are

A

insulin dependent

146
Q

if there is better A1C there will be

A

less complications

147
Q

type 2 metabolic abnormalities leading to

A

peripheral insulin resistance, deranged beta cell secretion of insulin, increased hepatic glucose production

148
Q

metabolic syndrome is ______ resistant

A

insulin

149
Q

metabolic syndrome includes ________ obesity

A

central

150
Q

metabolic syndrome people have ____________ which is increased triglycerides, low HDL

A

dyslipidemia

151
Q

metabolic syndrome have hyper ot hypo tension

A

hyper

152
Q

metabolic syndrome do or do not have atherloslcerosis

A

do

153
Q

metabolic syndrome has acanthuses nigricans which are

A

dark skin folds

154
Q

metabolic syndrome have what kind of inflammation

A

systemic chronic inflammation

155
Q

is gestational diabetes a small or large percent

A

small 5-10%

156
Q

how can we diagnose gestational diabetes

A

fasting plasma glucose >126 or random >200

157
Q

up to 60% of women with GDM will develop

A

type 2 diabetes after delivery

158
Q

a child that was born from a mom with GDM will

A

have an increase risk of developing type 2

159
Q

manifestations of type 1 are slow or rapid

A

rapid

160
Q

are manifestations of type 1 specific or nonspecific

A

very specific

161
Q

manifestations of type 2 are slow or rapid

A

slow

162
Q

manifestations of type 2 specific or nonspecific

A

nonspecific

163
Q

three polys that present with DM

A

polyuria, polydipsia, polyphagia

164
Q

glucose is a _______, osmotically active molecule

A

small

165
Q

high blood glucose levels exceeds amount that can be reabsorbs by _______ (aka renal threshold)

A

kidney

166
Q

the glucose exceeds renal threshold this causes

A

glycosuria and large water losses in urine

167
Q

intracellular dehydration causes

A

thirst

168
Q

cellular depletion of carbs, fats and proteins causes

A

hunger

169
Q

type 2 may present with

A

blurred vision, fatigue, paresthesias, skin infections

170
Q

polyuria is caused in DM because

A

glucose levels exceeds renal threshold

171
Q

polydipsia is caused in DM because

A

because urinating so much

172
Q

polyphagia is caused in DM because

A

glucose is not in the cell where it should be

173
Q

why can we not give insulin via mouth

A

it is destroyed in the GI tract

174
Q

DKA causes include

A

infection, inadequate use of insulin, pregnancy, stress

175
Q

DKA is a

A

metabolic acidosis

176
Q

DKA will present with deep breathing because of

A

compensation to the metabolic acidosis

177
Q

when a patient with DKA is breathing deep and hard what is this called

A

kussmaul breathing

178
Q

when blood pH decreases this causes decreased nerve firing which can lead to

A

confusion and coma

179
Q

when a patient has large amounts of ketones in their blood some patients are able to tell because of

A

acetone/fruity smell on breath

180
Q

if a patient is in DKA why would they be breathing heavy

A

R ALK

181
Q

if a patient is in DKA why would they be urinating so much

A

glucose has exceeded renal threshold

182
Q

if a patient is in DKA why would they be dehydrated

A

because they are losing fluid because of increased amounts of urination

183
Q

you find a man collapsed on the sidewalk and he is wearing a diabetic alert bracelet and has an insulin syringe in his brief case.
What happened?
Does he need insulin?
Why?
Hyper/hypo?

A

it happened suddenly so it is hypoglycemia. He does not need insulin he needs glucose/glucagon

184
Q

is DKA a slow or fast onset

A

slow

185
Q

DKA will have _________ tenderness

A

abdominal

186
Q

in DKA can or cannot patients tell if they are going through DKA

A

they can with an odor on their breath

187
Q

how will patients in DKA present BP and respiration wise?

A

hypotension and kussmaul breathing

188
Q

does hypoglycemia have slow or rapid onset

A

rapid

189
Q

when in hypoglycemia they will have altered _______ function and could lead to _____ and ________

A

cerebral, coma, seizures

190
Q

hypoglycemia will first have PNS which will present as

A

hunger

191
Q

in hypoglycemia after PNS is active then SNS will become active and present as

A

anxiety, tachycardia, sweating, skin cool/clammy

192
Q

in an elderly patient in hypoglycemia they may only present with ____ changes

A

CNS

193
Q

does a patient with HHS have a pH change

A

no

194
Q

HHS is characterized by hyperglycemia of

A

> 600

195
Q

HHS may mimic a

A

stroke

196
Q

HHS presents with (besides glucose count)

A

hyperosmolarity, dehydration, absence of ketoacidosis, depression of DNS

197
Q

DKA is normally in type

A

1

198
Q

HHS is normally in type

A

2

199
Q

somogyi effect

A

insulin induced hypoglycemia caused by a compensatory increase in catecholamines, glucagon, cortisol, and growth hormone which lead to hyperglycemia

200
Q

dawn phenomenom

A

hyperglycemia between 5A-9A with out following hypoglycemia

201
Q

if a patient who has known DM (don’t know what type) and their pH is 7.1
DKA or HHS

A

DKA

202
Q

if a patient who has known DM (don’t know what type) and their pH is 7.4
DKA or HHS

A

HHS

203
Q

if a patient who has known DM and their pH is 6.9, what type do they have

A

type 1 (DKA)

204
Q

if a patient who has known DM and their pH is 7.39 what type do they have

A

type 2 (HHS)

205
Q

nerve cells produce _________ ______ to keep their osmolarity balanced with the blood

A

intracellular osmoles

206
Q

DM can lead to chronic complications

A

diabetic neuropathies, nephropathies, retinopathies

207
Q

nephropathies can lead to

A

end stage renal diease

208
Q

retinopathies are the leading cause of acquired

A

blindness

209
Q

diabetic foot ulcers

A

impaired pain sensation contributes, risk of amputation if ulcers are not treated

210
Q

somatic neuropathies

A

diminished perception of vibration, pain and temp

211
Q

autonomic neuropathy

A

impaired motility of the gastrointestinal tract- gastroparesis

Pathophysiology (44 decks)

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