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Spring A 2025 > patho exam 2 > Flashcards

patho exam 2 Flashcards

1
Q

what is the function of thyroid hormones?

A

increases metabolism
increases protein synthesis
necessary or growth of children

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2
Q

disorders of the thyroid are among the _______ and affect how much of the US population?

A

they are among the most common endocrinopathies
they affect 4-5% of the population

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3
Q

what is the difference between the structure of T3 and T4?

A

a single atom of iodine

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4
Q

between T3 and T4, which is more active and which is released at a higher quantity?

A

T3 is more active
T4 is released in higher quantity

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5
Q

which (T3 or T4) is converted into the other?

A

T4 is converted into T3 once it reaches the target tissues

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6
Q

what does calcitonin do?

A

opposite action of parathyroid hormone
does NOT increase levels of calcium and phosphorus in blood
inhibits activity of osteoclasts and stops bone reabsorption

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7
Q

describe the structure of the thyroid gland

A

tiny saclike structures called follicles - func units
each follicle is formed by simply cuboidal epithelium

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8
Q

where are thyroid hormone made and stored?

A

they are made in the simple cuboidal cells of the thyroid and stored in the lumen attached to thyroglobulin

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9
Q

what are the 3 forms of thyroid hormones in the bloodstream?

A

bound to thyroxine-binding globulin
T4 binding prealbumin and albumin
free, unbound form - the active form

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10
Q

what enzyme converts T4 into T3?

A

5’-iodinase

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11
Q

what is a second form that T4 can be converted into?

A

reverse T3
a physiologically inactive form

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12
Q

actions of thyroid hormones in relation to GROWTH

A

growth formation
bone maturation

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13
Q

actions of thyroid hormones in relation to CNS

A

maturation of the CNS

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14
Q

actions of thyroid hormones in relation to BMR

A

increased Na-K ATPase
increased O2 consumption
increased heat production
increased BMR

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15
Q

actions of thyroid hormones in relation to METABOLISM

A

increased glucose absorption
increased glycogenolysis
increased gluconeogenesis
increased lipolysis
increased protein synthesis and degradation

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16
Q

actions of thyroid hormones in relation to CARDIOVASCULAR

A

increased cardiac output

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17
Q

define glycogenolysis

A

breakdown of glycogen to glucose

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18
Q

define gluconeogenesis

A

making of glucose from other products like amino acids or fats

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19
Q

what is goiter?

A

swelling of neck resulting from enlargement of the thyroid gland

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20
Q

what are the causes of goiter?

A

graves disease
TSH secreting tumor
iodine deficiency

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21
Q

what is hyperthyroidism?

A

tissues are exposed to high levels of circulating thyroid hormones

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22
Q

what are the causes of hyperthyroidism?

A

graves
adenoma of thyroid
excessive production of TSH by pituitary adenoma

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23
Q

how many people does graves disease affect?

A

0.5-1% of population under 40

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24
Q

what is graves disease and its triggering factors?

A

state of hyperthyroidism, goiter, opthalmopathy
excessive stimulation of thy gland by IgG antibodies

triggering factors:
often unknown
genetic - history, gender
environmental - stress, smoking

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25
Q

clinical manifestations of Graves disease

A

goiter
excessive sympathetic system activity
increased respiratory rate
increased DTRs
exophthalmos - bulging eyes
sweating, heat intolerance
increased appetite
weight loss
frozen shoulder
calcific tendinitis of the wrist

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26
Q

what is a thyroid storm?

A

sudden, worsening of hyperthy
high fever
server tachycardia
heart failure
irritability

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27
Q

what are the precipitating factors of thyroid storm?

A

trauma
infection
surgery
stress

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28
Q

diagnosis of graves

A

history
protrusion of eyes
TSH levels
elevated in serum T3/4
antithyroid antibodies
radioactive iodine uptake

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29
Q

treatment of graves

A

reducing thyroid hormone levels
medication that blocks thyroid hormone reproduction
surgical removal of gland

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30
Q

what is hypothyroidism?

A

deficient thyroid hormone
creates a generalized depression of body metabolism

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31
Q

describe congenital hypothyroidism

A

un utero hormones supplied by mother
if untreated after birth, intellectual disability
cretinism

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32
Q

describe acquired hypothyroidism

A

destruction of thy gland
impaired pit function
impaired hypothal function
iodine deficiency
autoimmunity that blocks TSH or TSH receptors - hashimoto thyroiditis

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33
Q

clinical manifestations of hypothyroidism

A

weakness and fatigue
weight gain, loss of appetite
cold intolerance
decreased GI motility
mental dullness
large tongue
peripheral edema
myxedema coma
delayed relaxation of DTR

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34
Q

clinical manifestations of hypothyroidism when myxedema is involved

A

carboydrate complexes accumulate and draw water into the tissue
fluffy face
tongue enlarged
voice hoarse
slurred speech
carpal tunnel syndrome

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35
Q

what other syndrome do those with hypothyroidism commonly develop?

A

fibromyalgia syndrome

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36
Q

diagnosis of hypothyroidism

A

history
T4 levels decreases
TSH levels increased

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37
Q

treatment of hypothyroidism

A

life long replacement therapy
levothyroxine - synthetic form of T4

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38
Q

what is the function of the parathyroid gland?

A

regulate Ca+ in ECF
secrete when CA+ levels fall
acts on bone, kidneys and intestine to increase plasma CA+ back to normal

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39
Q

what are the different forms of calcium in the blood?

A

total - 10mg/dl

40% bound to plasma proteins
10% bound to anions like phosphate, citrate
50% free, ionized Ca+

protein bound cannot be filtered

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40
Q

relationship between calcium and albumin

A

albumin has neg charge sites which can bind to ca+ or h+

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41
Q

what is hypercalcemia

A

increase in plasma Ca+ concentration
causes constipation, polyuria, polydipsia, hyporeflexia

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42
Q

what is hypocalcemia

A

decreased in plasma Ca+
causes muscle cramps, twitching, tingling, numbness, hyperreflexia

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43
Q

3 hormones of calcium hemostasis

A

PTH
calcitonin
vitamin D

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44
Q

actions of parathyroid hormone

A

bone remodeling
bone reabsorption
inhibits phosphate reabsorption
stims Ca+ reabsorption
activates vitamin D

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45
Q

when is calcitonin released?

A

increased plasma calcium concentration
released by thyroid gland

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46
Q

what is the function of calcitonin?

A

inhibits osteoclastic bone resorption
decreases plasma calcium concentration

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47
Q

what is the function of vitamin D?

A

regulates Ca+ and phosphate metabolism
reabsorb calcium from GI tract
promote mineralization of new bone

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48
Q

how is vitamin D synthesized?

A

D3 is ingested in diet or synthesized from skin

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49
Q

which vitamin D is active?

A

1,25-(OH)2-cholecalciferol

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50
Q

what is the action of vitamin D?

A

increases plasma phosphate and ca+
promote mineralization of new bone

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51
Q

if kidney cannot produce active vit D what happens?

A

it will all be inactive no matter how much is supplemented

52
Q

what is hyperparathyroidism?

A

over activity of one or more parathyroid glands
elevated PTH
affects women more

53
Q

what are the manifestations of hyperparathyroidism?

A

bone damage
hypercalcemia
hypertension
hypercalciuria
hypergastrinemia
diminished DTRs
kidney damage
glove stocking sensory damage

stones, bones, groans, psychiatric overtones

54
Q

diagnosis of hyperparathyroidism?

A

in the blood: increase PTH, hypercalcemia, hypophosphatemia

in urine: increased phosphate, increased ca+

55
Q

treatment of hyperparathyroidism

A

surgical removal
drugs to lower serum calcium
education for home safety

56
Q

what is hypoparathyroidism?

A

insuff secretion of PTH
causes low serum calcium levels and high serum phosphate levels

57
Q

what are the acquired causes of hypoparathroidism?

A

accidental removal
inadequate blood supply leading to infarction
TB
trauma
autoimmune

58
Q

what are the manifestations of hypoparathyroidism?

A

hypocalcemia
NM irritability
tetany
spasm
paraesthesia
cardiac arrhythmias

59
Q

what is Chvostek’s sign?

A

hypopara

hyperirri facial nerve when tapped

60
Q

what is trousseau sign?

A

carpal spasm when BP cuff inflated for over 3 min

61
Q

clinical manifestations of hypoparathyroidism

A

CNS - irri, anxiety, agitation, depression, seizures
CVS - arrhy, heart failure
dry scaly pigmented skin
thin hair and brittle nails
skin infections
nausea, vomiting
hypocalcemia: increased DTRs

62
Q

diag of hypoparathyroidism

A

low PTH, hypocalcemia, hyperphosphatemia

63
Q

treatment of hypoparathyroidism

A

aucte:
life threatening
need IV calcium
treat convulsions

chronic:
pharmacological
foods high in calcium and low in phosphorous

64
Q

what does the pancreas do?

A

endocrine gland: releasing hormones
exocrine gland: secreting digestive juices

65
Q

what are pancreatic islets?

A

clusters of endocrine cells in pancreas

66
Q

what are the 4 types of cells in the pancreas?

A

beta cells - secrete insulin
alpha cells - secrete glucagon
delta cells - secrete somatostatin

remaining secrete pancreatic peptide or other peptides

67
Q

what is insulin?

A

synthesized by beta cells
hormone of abundance
ensures that nutrients are stored correctly
A chain - 21 amino acids, B chain - 30 amino acids

68
Q

what is the order of synthesis of insulin?

A

proinsulin - A and B chains connected by connecting peptide
golgi apparatus cleaves out connecting peptide
insulin and c peptide are released in equal amounts

69
Q

what chromosome directs the synthesis of insulin

A

11

70
Q

where is glucose produced?

A

beta cells
GLUT2 transporter moves glucose from blood to cell
as calcium increases in beta cells, insulin goes out

71
Q

what can c peptide help monitor?

A

as it is unchanged in urine, it can monitor endogenous beta cell function
basis of test for T1D

72
Q

how does insulin effect nutrient flow?

A

decreases blood glucose levels
decreases blood fatty acids and ketone concentrations
decreases blood amino acid concentration
ensures ingested K+ will be taken into cells

73
Q

what are the different actions of glucose?

A

increases glucose uptake in cells
increases glycogen formation
decreases glycogenolysis
decreases gluconeogenesis
increases protein synthesis
increases fat deposition
decreases lipolysis
increases K+ uptake into cells

74
Q

what is glucagon?

A

it is synthesized and secreted by alpha cells
hormone of starvation
maintains blood glucose concentration in fasting state

75
Q

what are the major actions of glucagon on the liver?

A

increases blood glucose concentration
- stimulates glycogenolysis
- inhibits glycogen formation from glucose
- increases gluconeogenesis
increases blood fatty acid and ketoacid concentration
- increases lipolysis

76
Q

what is somatostatin?

A

secreted by delta cells of islet and hypothalamus

77
Q

what is the action of somatostatin?

A

modulate or limit the response of insulin and glucagon to ingestion of food
inhibits the release of GH, TSH and prolactin

78
Q

if you skipped breakfast and had really low blood glucose levels, which cells of islet would you expect the be stimulates?

A

alpha cells

79
Q

what is diabetes mellitus?

A

increased blood glucose levels (hyperglycemia)
disruption of metabolism of carbohydrate, proteins, fats

80
Q

what is the 7th leading cause of death in the US?

A

diabetes

81
Q

glucose homeostasis

A

blood glucose rises, beta cells release insulin, body cells taken up more glucose and liver stores glucose as glycogen, blood glucose levels decline

blood glucose levels fall, alpha cells release glucagon, lever breaks down glycogen and releases glucose, blood glucose level rises

82
Q

what are the two types of diabetes?

A

type 1 - insulin dependent diabetes mellitus
type 2 - no insulin dependent diabetes mellitus

83
Q

in adults, what percentage of diabetes cases are T1D/T2D?

A

T1D- 5-10%
T2D - 90-95%

84
Q

when does T1D commonly develop?

A

most common onset in childhood or adolescence

85
Q

what is T1D?

A

autoimmune destruction of beta cells
progress can be slow or rapid

86
Q

what is prediabetes?

A

early stages of immune destruction
antibodies against beta cells circulating, but not hyperglycemic yet
can last for years

87
Q

when does T1D manifest?

A

80-90% of beta cell destruction

88
Q

manifestations of T1D

A

sudden
blurred vision
fatigue
skin infection
polyuria
fatigue
weight loss
polyphagia
polydipsia

89
Q

what is diabetic ketoacidosis?

A

metabolic derangement seen more in T1D
ketones detected in blood and urine
produce hydrogen ions - metabolic acidosis
protein catabolism

90
Q

treatment of T1D: exogenous insulin types

A

rapid acting - onset 15 min, immediately before meal
short acting - 30 min, throughout day
intermediate acting - 2-4 hors, throughout day
long acting - 6-10 hrs, nighttime
other - 2-4 hrs, nighttime

normally one shorter acting and one longer acting

91
Q

what are the ways someone can take insulin?

A

syringes
insulin pen
insulin pump

92
Q

treatment of T1D

A

exogenous insulin
transplant of pancreatic islets
- at least 2-3 donors needed
diet
exercise

93
Q

when does T2D onset?

A

late in life
associated with obesity and PI, genetic susceptibility

94
Q

who is at high risk for T2D?

A

age greater or equal to 45 yrs old
hypertension
positive family history
HDL chol <35 mg/dl
triglycerides greater or equal to 250 mg/dl
obesity
sed lifestyle
cigarette smoking

95
Q

pathophysiology of T2D

A

insulin is present but not used by tissues
beta cells gradually fail
normally diagnosed while being treated for something else

96
Q

what is the diagnostic criteria for T2D?

A

random BG levels equal to or more than 200 mg/dl
fasting BG levels
2 hour glucose tolerance test
HbA1c-glycated Hb

97
Q

what is the normal level for fasting blood glucose levels?

A

<100mg/dl

98
Q

what is the prediabetes level for fasting blood glucose levels?

A

100-125 mg/dl

99
Q

what is the diabetes level for fasting blood glucose levels?

A

greater to equal to 126 mg/dl

100
Q

what is the normal level for HbA1c levels?

A

<5.7%

101
Q

what is the prediabetes level for HbA1c levels?

A

5.7 - 6.4%

102
Q

what is the diabetes level for HbA1c levels?

A

greater than or equal to 6.5%

103
Q

what is the normal level for oral glucose tolerance test levels?

A

< 140 mg/dl

104
Q

what is the prediabetes level for oral glucose tolerance test levels?

A

140-199 mg/dl

105
Q

what is the diabetes level for oral glucose tolerance test levels?

A

greater than or equal to 200 mg/dl

106
Q

diagnostic criteria for diabetes

A

FPG greater than or equal to 126 mg/dl
2-hr PG greater than or equal to 200 mg/dl in OGTT
A1C greater than or equal to 6.5%
random plasma plasma glucose greater or equal to 200mg/dl

107
Q

laboratory tests for T2D

A

glucose present in urine
ketones present in urine
presence of antibodies against islet cells

108
Q

manifestations of T2D

A

insidious
blurred vision
fatigue
skin infections
polyuria
fatigue
polydipsia

109
Q

complications of long-term diabetes: leading cause of

A

blindness
chronic kidney disease
lower extremity amputations

all organs are effected

110
Q

complications of long term diabetes

A

macrovascular:
atherosclerosis
reduced blood flow
gangrene
limb amputation

microvascular:
low blood flow
ESRD

foot ulcers
susceptible to infections
loss of sensation
weakness and atrophy
loss of control of blood pressure, temp, sweating
UTI

111
Q

MSK problems associated with long term diabetes

A

dupuytren’s contracture
flexor tenosynovitis
trigger finger
carpal tunnel syndrome
adhesive capsulitis
tendinopathy with thickening of plantar fascia, achilles
osteoporosis

112
Q

treatment of T2D

A

medications:
alpha-glucosidase inhibitors - slows carb digestion
biguanides (metformin) - prevents excess glucose release from liver
meglitinides - more secretion of insulin
sulfonylureas - more secretion of insulin
thiazlidinediones - increases sensitivity to tissues to insulin

diet
excerise

113
Q

what are the extreme complications of hypoglycemia?

A

< 70 mg/dl

shakiness
pale skin color
cold clamy skin
dizziness
sweating
clumsy/jerky movements
hunger
seizure
headache
increased HR
coma - below 50 mg/dl

114
Q

what are the extreme complications of hyperglycemia?

A

> 300 mg/dl with ketones
ketones with one or more of the following require ER

DKA: rate and depth of respiration increases
marked fatigue
nausea and vomiting
breath that smells fruity
a very dry mouth

115
Q

what are the extreme BG levels where you do not do therapy?

A

< 70 mg/dl
>250 with ketones

116
Q

what are the complications of diabetes treatment?

A

overdose of insulin
skipped meals
overexertion in exercise
excessive alcohol ingestion
change in meds

117
Q

when does a person need to be hospitalized for hypoglycemia?

A

< 50 g/dl

118
Q

how can a person become hypoglycemic?

A

overdose on insulin
skipped meals
overexertion in exercise
excessive alcohol ingestion
change in meds

119
Q

what is the somogyi phenomenon?

A

increased fasting blood glucose levels during early morning that is triggered by preceding hypoglycemic event

cause:
large insulin doses
skipped meals
heavy exercise

120
Q

what is the dawn phenomenon?

A

increased fasting blood glucose in the early morning not triggered by hypoglycemic event

more common
result of circadian variation in hormone secretion

121
Q

what is gestational diabetes?

A

during pregnancy
usually temporary
insulin resistance and inability to create more insulin

risk of c section due to large baby

122
Q

what percent of pregnancies develop gestational diabetes?

A

15%

diag in 5-6th month

123
Q

treatment of gestational diabetes

A

diet
exercise
drugs/insulin

124
Q

what happens if gestational diabetes is untreated?

A

developmental abnormalities like spina bifida
heart defects
large body size of baby

125
Q
A

Spring A 2025 (6 decks)

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