Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ENDOREPRO MODULE > ENDOREPRO PATHPHYSIO > Flashcards

ENDOREPRO PATHPHYSIO Flashcards

1
Q

What are the principle mammographic signs of breast carcinomas?

A

Densities and calcifications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Acute Mastitis

A

Erythematous, Painful, Fever
Almost all cases occur in first month of breastfeeding
Staph aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Periductal Mastitis AKA subareolar abscess

A

painful erythematous subareolar mass
most people afflicted are smokers
many women have inverted nipple
keratinizing squamous metaplasia of the nipple ducts; keratin sheds -> plugs duct -> dilation and rupture ->intensive inflammatory respons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Mammary Duct Ectasia

A

poorly defined palpable periareolar mass -> mimics a carcinoma on mammography
thick, white nipple secretions,
multiparous women in 5-6 decade of life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Fat Necrosis

A

painless palpable mass
skin thickening or retraction
mammographic density or calcifications
history of breast trauma or prior surgery,
significance is confusion with breast cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Lymphocytic Mastopathy

A

hard palpable masses,
collagenized stroma surrounding atrophic ducts and lobules
common in women with Type 1 diabetes or autoimmune thyroid disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Granulomatous Mastitis

A

Causes: systemic granulomatous diseases that occas. involve breast and granulomatous infections caused by mycobacteria or fungi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Benign Epithelial Lesions divisions

A

1) nonproliferative breast changes
2) proliferative breast disease
3) atypical hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Nonproliferative Breast Changes (Fibrocystic changes)

A

1) cystic change, often with apocrine metaplasia, 2)fibrosis, 3) adenosis
do not increase risk of cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Proliferative Breast Disease without Atypia

A

proliferation of ductal epitheliam and/or stroma without cytologic or architectural features suggestive of CIS
Epithelial Hyperplasia; Sclerosing Adenosis; Complex Sclerosing Lesion; Papillomas
mild increase risk of cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Proliferative Breast Diseas with Atypia

A

Atypical Ductal Hyperplasia; Atypical Lobular Hyperplasia;

moderate increase risk of cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Thyroglossal Duct Cyst
Description
Presentation

A

Cystic dilation of thyroglossal duct remnant

Presents as anterior neck mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Lingual Thyroid

Presentation

A

Presents as base of tongue mass.

Persistence of thyroid tissue at base of tongue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hyperthyroidism:
D
PP (Pathophysiology)

A

D:Increased level of circulating thyroid hormone.
P: Increases BMR (Na-K ATPase), Increases sympathetic nervous system activity (B-adrenergic receptors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hyperthyroidism

CP

A 
Weight loss
Increased appetite
Heat intolerance and sweating
tachycardia with increased CO
arrhythmia
Tremor, anxiety, insomnia, heightened emotions, diarrhea w/ malabsorption, bone resorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

When a patient gets hyperthyroidism, what happens to cholesterol and glucose levels in the serum?

A

Hypocholesterolemia

Hyperglycemia (thyroid hormone promotes gluconeogenesis and glycogenolysis -> extra sugar in the blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Graves Disease:
Most common cause of what?
D
PP

A

Most common cause of HYPERTHYROIDISM.
Autoantibody (IgG) that stimulates TSH receptor.
Leads to increased synthesis and release of thyroid hormone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Graves Disease

CP

A

hyperthyroidism
diffuse goiter
exophalmos and pretibial myxedema (myx- glycoseaminoglycans)
-fibroblasts in eye and shin have TSH receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Graves Disease

Histology

A

“scalloping of the colloid”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q 
Graves Disease Lab Findings
T4
TSH
Cholesterol
glucose?
A

Increase in total and free T4
Decrease in TSH
Hypocholesterolemia
Increased serum glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Treatment for Graves Disease

A

B-blockers
Thiomide
Radioiodine ablation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the “Thyroid Storm?”

A

Elevated catecholamines and massive hormone excess (stress)
Present with arrhythmia, hyperthermia, and vomiting with hypovolemic shock
Treated with PTU, B-blockers and steroids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Multinodular Goiter:
Description
Cause

A

Enlarged thyroid gland with multiple nodules
Due to relative iodine deficiency
Usually nontoxic (euthyroid)
Rarely, regions become TSH-independent (“toxic goiter”)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Cretinism?
What is it?
Clinical Findings?

A

hypothyroidism in neonates or infants
Findings: mental retardation, short stature with skeletal abnormalities, coarse facial features, enlarged tongue, umbilical hernia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Cretinism Causes

A

Maternal hypothyroidism during early pregnancy
Thyroid Agenesis
Dyshormonogenetic goiter (most common enzyme that is deficient is thyroid peroxidase)
Iodine deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Myxedema Disease:

What is it?

A

Hypothyroidism in older children or adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Clinical features of Myxedema:

A

Myxedema (larynx and large tongue)
Weight gain despite normal appetite; slowing of mental activity, hypercholesterolemia, constipation,bradycardia with decreased CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Causes of hypothyroidism in adults?

A

Iodine deficiency
Hashimoto thyroiditis
Drugs (lithium)
surgical removal or radioablation of thyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Hashimoto Thyroiditis:

What is it the most common cause of?

A

Most common cause of hypothyroidism where iodine levels are sufficient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What antigen is Hashimoto Thyroiditis assoc. with?

A

HLA-DR5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

PP of Hashimoto thyroiditis

A

Autoimmune destruction of the thyroid gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Hashimoto Thyroiditis

CP

A

Initially present with hyperthyroidism (destroyed colloid -> leads to leaking of thyroid hormone)
then progresses to hypothyroidism: dec. T4 and inc. TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What hormone controls the number of TRH receptors on the anterior pituitary?

A

T4; less T4 -> more TRH receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Hashimoto Thyroiditis

Histology

A

Germinal Centers!
Chronic Inflammation
Herthle Cell change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What do patients with Hashimoto Thyroiditis have an increased risk of developing?

A

B-cell lymphoma -> present with enlarging thyroid gland with HT
Germinal Centers generate post germinal center B cells -> marginal zones -> marginal zone lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Subacute (deQuervain Granulomatous Thyroiditis)
Cause?
Presentation?

A

Granulomatous thyroiditis that follows a viral infection
Presents as tender thyroid with transient hyperthyroidism
Self-limited; does not progress to hypothyroidism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Woman has a tender thyroid, what is the first diagnosis to consider?

A

Subacute (deQuervain Granulomatous Thyroiditis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Reidel Fibrosing Thyroiditis
What is it?
Key “phrase” in a question stem?

A

Chronic inflammation with extensive flibrosis of thyroid
Presents as hypothyroidism with HARD AS WOOD, NON TENDER THYROID GLAND.
Fibrosis can extend to local areas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Are thyroid nodules likely to be benign or malignant?

A

Benign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the key mechanism to sampling the thyroid?

A

FNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Increased uptake of 131-I is seen it what diseases?

A

Usually benign conditions, such as Graves or nodular goiter.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Decreased uptake of 131-I is seen in what conditions?

A

It can be benign or malignant.

Adenoma and carcinoma are decreased uptake.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Follicular Adenoma

Histology

A

Tumor is making follicles, but there is a dense pink capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Four types of Thyroid Carcinoma?

A

Papillary, Follicular, Medullary, Anaplastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Most common type of thyroid carcinoma?

A

papillary carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Major risk factor for papillary carcinoma?

A

Exposure to ionizing radiation in childhood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Papillary Carcinoma

Histology

A

Papillary finger like projections
Nuclear features define carcinoma: orphan Annie eyed nuclei (white clearing in the center of nucleus)
Nuclear grooves
Psammoma body (concentric layered calcification)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Follicular Carcinoma?

malignant proliferation of what? How do you differentiate between an adenoma?

A

Malignant proliferation of follicles

Surrounded by fibrous capsule with INVASION through capsule.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

FNA can or cannot distinguish between follicular adenoma and carcinoma?

A

CANNOT, you need to examine the capsule.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How does follicular carcinoma spread?

A

Hematogenously. Usually carcinomas spread by lymph nodes besides a few, but not this carcinoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Medullary carcinoma.
Proliferation of what type of cell?
What hormone would you have high levels of?

A

Malignant proliferation of parafollicular C-cells

High levels of calcitonin produced by tumor may lead to hypocalcemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Medullary carcinoma of the thyroid.

Histology

A

Calcitonin often deposits within tumor as amyloid (localized amyloidosis).
Malignant tumor cells within amyloid stroma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Familial cases of medullary carcinoma of the thyroid are associated with what mutation?

A

Often due to MEN 2A and 2B
Associated with mutations in RET oncogene.
Detection of RET mutation warrants prophylactic thyroidectomy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Name the three common MEN 2A neoplasms.

A

Medullary carcinoma of the thyroid
Pheochromocytoma
Parathyroid Adenomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Name the three categories of common neoplasms associated with MEN 2B.

A

Medullary carcinoma of the thyroid.
Pheochromocytoma.
Mucosal ganglio-neuromas, particularly of oral mucosa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Aplastic carcinoma of the thyroid?
Description.
Who usually gets it?

A

Undifferentiated malignant tumor of the thyroid
Usually seen in elderly
Often invades local structures leading to dysphagia or respiratory compromise.
POOR prognosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How do you differentiate between Reidel Fibrosing Thyroiditis and Aplastic carcinoma of the thyroid?

A

Reidel is usually seen in younger patients, and aplastic carcinoma is usually seen in the elderly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the key cell in the parathyroid gland called? What is it’s purpose?

A

Chief cell

Regulate serum free (ionized) calcium via PTH secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the most common cause of primary hyperparathyroidism?

A

Parathyroid adenoma (>80% of cases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the consequences of increased PTH and hypercalcemia?

A

Nephrolithiasis
Nephrocalcinosis -> renal insufficiency with polyuria
CNS disturbances -> depression and seizures
Constipation, peptic ulcer disease, and acute pancreatitis
Osteitis fibrosa cystica (because of massive resorption of bone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Lab findings in hyperparathyroidism?

A 
High serum PTH
Low serum P
High serum calcium
Increased urinary cAMP (ATP -> cAMP cascade)
Inc serum Alk Phos
62
Q

What is the most common cause of secondary hyperparathyroidism?

A

Chronic Renal Failure.
Renal failure -> dec excretion of P -> P binds to free Calcium -> free calc levels decrease -> stimulate parathyroid glands to increase PTH secretion

63
Q

Lab findings of secondary hyperparathyroidism

A

High PTH
Low serum calcium
Inc serum phosphate
Inc alkaline phosphatase

64
Q

Hypoparathyroidism causes

A

Autoimmune damage, surgical excision, DeGeorge syndrome

65
Q

Hypoparathyroidism CP

A

numbness and tingling
muscle spasms (tetany)
Dec PTH and dec serum Ca

66
Q

Pseudohypoparathyroidism description

A

Due to end-organ resistance to PTH

Hypocalcemia with HIGH PTH levels

67
Q

Why do Cushing syndrome patients have moon facies, buffalo hump, truncal obesity?

A

High glucose -> excess insulin -> storage of fat

68
Q

Why do Cushing syndrome patients have abdominal striae?

A

Cortisol inhibits the synthesis of collagen -> weak collagen -> blood vessels rupture easily

69
Q

Why do Cushing syndrome patient’s have hypertension?

A

Cortisol upregulates Alpha 1 receptors on the arterioles -> increases effect of NE. Cortisol helps maintain vascular tone by this method. Excess cortisol will cause increased effect of NE… HT

70
Q

Cortisol is used as an immunosuppressant in three major ways. Describe

A

1) inhibit phospholipase a2 -> cannot generate arachidonic acid metabolites
2) inhibits IL-2, important T-cell growth factor
3) inhibits release of histamine from mast cells -> histamine is essential for vasodilation and vascular permeability.

71
Q

How do you diagnose Cushing syndrome?

A

increased 24 hr urinary cortisol level

72
Q

What is the most common cause of Cushing syndrome?

A

Exogenous corticosteroids -> leads to atrophy of BOTH adrenals

73
Q

When comparing the adrenal glands, will they be the same size or different size with a primary adrenal adenoma, hyperplasia or carcinoma?

A

Different size. One tumor will be excessively secreting cortisol and get larger and the other will atrophy.

74
Q

What will a high-dose dexamethasone test determine?

A

Dexamethasone will suppress ACTH production by a pituitary adenoma, but will fail to suppress ectopic ACTH production by a small cell lung carcinoma.

75
Q

What happens to Na, K and Hydrogen ion in response to aldosterone?

A

Sodium is absorbed, K is excreted and Hydrogen ion is excreted.

76
Q

Hyperaldosteronism effects?

A

Hypernatremia
Hypokalemia
Metabolic Alkalosis
Patient will also have hypertension

77
Q

Most common cause of Primary hyperaldosteronism?

A

adrenal adenoma

characterized by high aldosterone and low renin

78
Q

Secondary hyperaldosteronism cause?

A

Activation of the renin-angiotensin system (JGA apparatus activated by some form of sclerosis) -> renin secreted (angiotensinogen to angiotensin I -> 1 to 2 -> aldosterone activation

79
Q

If a patient has all of the classic signs for 21-hydroxylase deficiency but does NOT have salt wasting, hypovolemia or hyperkalemia, what is another possible diagnosis?

A

CAH from 11-hydroxylase deficiency

80
Q

What are signs and symptoms of a 17-hydroxylase deficiency for CAH?

A

No cortisol or sex steroid production, excess mineralocorticoids.
Always no cortisol, so excess ACTH leading to CAH.

81
Q

Waterhouse-Friderichsen syndrome clinical presentation:

A

Acute insufficiency of the adrenal glands -> lack of adrenal hormones.
Classic: young child, N. meningitidis infection, DIC, atrophy of adrenal glands, massive hypotension due to lack of cortisol.

82
Q

“Sack of blood” adrenal gland on gross examination in characteristic of what condition?

A

Waterhouse-Friderichsen syndrome

83
Q

What are the three major causes of chronic insufficiency of the adrenal glands?

A 
Autoimmune destruction -> developed world
TB -> developing world
Metastatic carcinoma (LUNG CANCER LOVES TO GO TO THE ADRENAL)
84
Q

Chronic Renal insufficiency clinical features?

A

Hypotension (cortisol)
Hyponatremia, Hyperkalemia, hypovolemia (aldosterone)
Weakness
Hyperpigmentation (cortisol due to excess ACTH)
Vomiting and Diarrhea (cortisol)

85
Q

ACTH is derived from what molecule?

A

POMC

Derivative of POMC is melanocyte stimulating hormone (MSH)

86
Q

Chromaffin cells are derived from what embryologic component? Where are they located? What is their physiologic function?

A

Neural crest
Adrenal Medulla
Main physiologic source of catecholamines (E and NE)

87
Q

Pheochromocytoma is a tumor of what? Describe the gross and histological presentation.

A

Chromaffin cells

Brown Tumor because adrenal medulla is brown

88
Q

Clinical features of a pheochromocytoma?

A 
Episodic HTN
Headaches
Palpitations
Tachycardia
Sweating
89
Q

How do you diagnose a pheochromocytoma? Treatment?

A

Increased serum metanephrines
Increased 24-hr urine metanephrines and VMA
(Epi is broken down to metanephrine, NE down to normetanephrine… both broken down to VMA by monoamineoxidase)
Treatment: surgical excision, but give patient phenoxybenzamine before!! to avoid surge of NE and E.

90
Q

Rules of 10 is referring to what condition? What are they?

A 
Pheochromocytoma
10% bilateral
10% familial
10% malignant
10% located outside adrenal medulla (bladder wall)
91
Q

What are conditions associated with pheochromocytoma?

A

MEN2A and 2B
VHL disease
NF type 1

92
Q

What is the classic presentation of Toxic multinodular goiter?

A

Older adult with history of nontoxic multinodular goiter.

May have cardiac complications such as a.fib and/or heart failure

93
Q

Thyroiditis is typically caused by what? If tissue inflammation and destruction occurs, what can be the result?

A

Typically caused by viral infection but broad differential (could also be hashimoto thyroiditis).
Release of preformed thyroid hormone, leading to transient thyrotoxicosis.

94
Q

What does thyrotoxicosis mean?

A

Excess of thyroid hormone in the body

95
Q

What are potentially permanent causes of thyrotoxicosis?

A

Graves Disease, Toxic multinodular goiter, Toxic adenoma, pituitary adenoma

96
Q

What are some transient causes of thyrotoxicosis?

A 
Hashimoto Thyroiditis
Subacute thyroiditis (de Quervain thyroiditis)
Iodine-induced (jodbasedow effect)
97
Q

If a patient has unintentional weight loss with a preserved or increased appetite, what three diagnosis should one consider?

A

Hyperthyroidism
Diabetes Mellitus
Malabsorption syndrome

98
Q

What is myxedema coma?

A

sever manifestation of hypothyroidism. Patients may present with profound lethargy or coma, weakness, hypothermia, and hypoglycemia.
Emergent treatment may require T3 and T4 (but need to give steroids before to prevent adrenal crisis!)

99
Q

Differential Diagnosis of Hypothyroidism?

A 
Endemic Cretinism (I deficient)
Endemic Goiter (I deficient)
Hashimoto Thyroiditis
Iatrogenic (thyroidectomy)
Riedel thyroiditis (chronic fibrosis)
de Quervain thyroiditis (viral in nature)
100
Q

What are two anabolic actions of GH?

A

Promotes tissue growth of MS system and visceral organs

Stimulates liver to secrete IGF-1

101
Q

What is acromegaly?

A

Hormonal disorder that develops when your pituitary gland produces too much GH during adulthood. Transverse bone growth in response to GH can continue throughout adulthood.

102
Q

What hormone does dopamine inhibit?

A

Prolactin

103
Q

What are the three metabolic actions of GH?

A

Skeletal Muscle - enhance protein synthesis
Adipose tissue - promote fat metabolism
Liver - Preserve body carbohydrate by gluconeogenesis and preventing glucose utilization by peripheral tissues so that they are forced to burn fats.

104
Q

What processes stimulate GHRH release from the hypothalamus?

A

Fasting, Sleep, Hypoglycemia, Stress!

105
Q

Where is GH secreted and from what type of cell?

A

Pituitary, somatotroph

106
Q

What hormone inhibits GH release?

A

Somatostatin

107
Q

Liver IGF inhibits secretion of what hormones?

A

Feedback inhibition of GHRH and GH

108
Q

What is a growth-hormone suppression test?

A

Oral load of glucose is rapidly administered -> increases plasma glucose levels -> which SHOULD inhibit GH secretion and IGF-1 in healthy adult.
If plasma GH levels do not decrease to less than 2 ng/mL in response to glucose load, GH HYPERSECRETING PITUITARY ADENOMA is indicated.

109
Q

What will happen if you administer insulin to a patient who is suspected to have GH hyposecretion.

A

GH will fail to secrete despite the provoked hypoglycemia and is evidence of a pituitary GH hyposecretion or panhypopituitarism, or both.

110
Q

Hyperglycemia inhibits or stimulates GH secretion?

A

Inhibits.

111
Q

What is octreotide?

A

Synthetic somatostatin analogue.

Treats GH-secreting tumors of the anterior pituitary.

112
Q

What does an absence of ADH lead to?

A

Dilution of urine

Loss of free water

113
Q

What are some of ADH’s physiological actions?

A

stimulates FREE WATER reabsorption by kidneys (concentrates urine), increases plasma volume, decreases plasma osmolarity
High concentrations, promotes systemic vasoconstriction -> increased arteriole BP

114
Q

What regulates ADH secretion?

A

Hypothalamic osmoreceptors -> shrink or swell by changing plasma osmolarity

115
Q

What triggers ADH secretion?

A

Increased plasma osmolarity

Decreased plasma volume

116
Q

Central DI pathophysiology?

A

Deficiency of functional ADH

117
Q

Nephrogenic DI pathophysiology?

A

Tissue insensitivity (collecting tubule) to circulating ADH

118
Q

What is the classic presentation of DI?

A

Production of large volumes of dilute urine as a result of the inability of kidneys to reabsorb water and concentrate urine
*kidneys are always diluting, never concentrating urine –> thats why we need ADH!

119
Q

Will central or peripheral DI respond to administration of synthetic ADH?

A

Central

120
Q

What is a common cause of nephrogenic DI?

A

Long term lithium use

121
Q

What are some common causes of Central DI?

A

Head Trauma
Hypothalamic Lesions
Neoplasms
Gene mutations in vasopressin gene

122
Q

What is another name for ADH?

A

arginine vasopressin; vasopressin

123
Q

If synthetic ADH is administered to a patient with central DI, what will happen to their urine?

A

It will become concentrated

124
Q

If a patient has pathological increased levels of ADH, what will happen to the plasma osmolarity?

A

Plasma osmolarity will be reduced and dilutional hyponatremia will occur.

125
Q

What is the condition in which the patient is always concentrating urine and never diluting urine?

A

SIADH ( Syndrome of inappropriate antidiuretic hormone secretion)
Urine will be inappropriately concentrated given the low plasma sodium concentration.

126
Q

What are oxytocin’s functions?

A

Promotes uterine contraction in response to dilation of cervix during labor.
Stimulates contraction of myoepithelial cells of breast in response to suckling during breastfeeding.
Secretion stimulated by sight and sounds of a newborn.

127
Q

B-cells lie in what portion of the islets?

A

The center of the islets

128
Q

What receptor is up regulated by insulin in skeletal muscle?

A

GLUT4 allowing glucose to enter into those tissues

129
Q

What is the pathophysiology of DM Type I?

A

Autoimmune destruction of B-cells by T lymphocytes

Inflammation of the islets

130
Q

What MHC Class II cell surface receptors are associated with Diabetes Mellitus Type I?

A

HLA-DR3 and HLA-DR4

Can also have autoantibodies against insulin in blood

131
Q

Why will patients have weight loss and low muscle mass in DM Type 1?

A

The patients have unopposed glucagon –> leading to gluconeogenesis and requiring energy (a.a.) so there will be glycogenolysis, lipolysis and breaking down muscle.

132
Q

How does DKA usually arise?

A

Often arises with stress or infection. Epi will increase glucagon exacerbating lipolysis (FREE FATTY ACIDS), gluconeogenesis and glycogenolysis —> FFA will go to liver and will be converted to ketone bodies —> Diabetic ketoacidosis

133
Q

What are the ketone bodies?

A

B-hydroxybutyric acid, acetoacetic acid, acetone.

134
Q

Clinical features of DKA?

A

Hyperglycemia ( >300 mg/dL)
Anion gap metabolic acidosis (ketoacids floating in blood)
Hyperkalemia (insulin drives K into cells, no insulin = K outside of cells; acidosis -> buffer mechanism bring H in and K out) but the patients are still excreting K.
Kussmaul respirations, dehydration, nausea, vomiting, mental status changes, fruity smelling breath.

135
Q

Treatment for DKA??

A

Fluid
Insulin
Replacement of electrolytes (potassium)

136
Q

Besides glucose, insulin also drives what metabolite into cells?

A

potassium

137
Q

Type II DM Pathophysiology?

A

End-organ insulin resistance -> metabolic disorder characterized by hyperglycemia.

138
Q

Which has a stronger genetic predisposition, Type 1 or Type 2 DM?

A

Type 2 Diabetes Mellitus

139
Q

What are histologic features for DM Type II?

A

Islets will become full of amyloid

140
Q

Describe quantitatively the levels of insulin for a DM Type II patient.

A

Initially the insulin will increase due to the increased insulin resistance but then the islet cells will get exhausted and insulin levels will decrease and lead to insulin deficiency

141
Q

Clinical features of DM Type II

A

Polyuria
Polydipsia
Hyperglycemia
Often clinically silent

142
Q

Treatment for DM Type II?

A

Weight Loss (Diet and Exercise)
Drug therapy to counter insulin resistance
Insulin in the later stages of the disease.

143
Q

What are DM Type II patients at risk for developing? What is the cause of it?

A

Hyperosmolar non-ketogenic coma.
High glucose levels (>500 mg/dL) leads to life threatening diuresis
Hypotension and coma
Ketones are absent!

144
Q

What does NEG stand for?

A

Non enzymatic glycosylation

145
Q

What are some complications from NEG of vascular BM? What patients are at risk?

A

Diabetes Mellitus Type II!
NEG of large- and medium- sized vessels –> atherosclerosis.
NEG of small vessels -> hyaline arteriolosclerosis
NEG of hemoglobin -> HbA1c

146
Q

What cells can take up sugars without the need for insulin?

A

Schwann Cells
Pericytes of retinal blood vessels
Lens

147
Q

What enzyme converts glucose to sorbitol?

A

aldose reductase

148
Q

MEN 1 neoplasms?

A

Pituitary Adenoma
Pancreatic Endocrine tumor (tumor of islet cells)
Parathyroid hyperplasia

149
Q

Insulinoma lab findings for glucose, insulin and C-peptide

A

Decrease glucose
Increase insulin
Increase C-peptide

150
Q

What should you consider if a patient has high insulin but not an increase in C-peptide?

A

Malingering, the patient is injecting insulin into themselves since C-peptide is produced with insulin within the body.

151
Q

Episodic hypoglycemia with mental status changes that are relieved by glucose. Possible Diagnosis to consider?

A

Insolinoma

ENDOREPRO MODULE (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions