ENDOREPRO PATHPHYSIO Flashcards
1
Q
What are the principle mammographic signs of breast carcinomas?
A
Densities and calcifications
2
Q
Acute Mastitis
A
Erythematous, Painful, Fever
Almost all cases occur in first month of breastfeeding
Staph aureus
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
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
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
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
7
Q
Granulomatous Mastitis
A
Causes: systemic granulomatous diseases that occas. involve breast and granulomatous infections caused by mycobacteria or fungi
8
Q
Benign Epithelial Lesions divisions
A
1) nonproliferative breast changes
2) proliferative breast disease
3) atypical hyperplasia
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
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
11
Q
Proliferative Breast Diseas with Atypia
A
Atypical Ductal Hyperplasia; Atypical Lobular Hyperplasia;
moderate increase risk of cancer
12
Q
Thyroglossal Duct Cyst
Description
Presentation
A
Cystic dilation of thyroglossal duct remnant
Presents as anterior neck mass
13
Q
Lingual Thyroid
Presentation
A
Presents as base of tongue mass.
Persistence of thyroid tissue at base of tongue.
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)
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
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)
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.
18
Q
Graves Disease
CP
A
hyperthyroidism
diffuse goiter
exophalmos and pretibial myxedema (myx- glycoseaminoglycans)
-fibroblasts in eye and shin have TSH receptor
19
Q
Graves Disease
Histology
A
“scalloping of the colloid”
20
Q
Graves Disease Lab Findings T4 TSH Cholesterol glucose?
A
Increase in total and free T4
Decrease in TSH
Hypocholesterolemia
Increased serum glucose
21
Q
Treatment for Graves Disease
A
B-blockers
Thiomide
Radioiodine ablation
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.
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”)
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
25
Cretinism Causes
Maternal hypothyroidism during early pregnancy
Thyroid Agenesis
Dyshormonogenetic goiter (most common enzyme that is deficient is thyroid peroxidase)
Iodine deficiency
26
Myxedema Disease:
| What is it?
Hypothyroidism in older children or adults
27
Clinical features of Myxedema:
Myxedema (larynx and large tongue)
Weight gain despite normal appetite; slowing of mental activity, hypercholesterolemia, constipation,bradycardia with decreased CO
28
Causes of hypothyroidism in adults?
Iodine deficiency
Hashimoto thyroiditis
Drugs (lithium)
surgical removal or radioablation of thyroid
29
Hashimoto Thyroiditis:
| What is it the most common cause of?
Most common cause of hypothyroidism where iodine levels are sufficient
30
What antigen is Hashimoto Thyroiditis assoc. with?
HLA-DR5
31
PP of Hashimoto thyroiditis
Autoimmune destruction of the thyroid gland
32
Hashimoto Thyroiditis
| CP
Initially present with hyperthyroidism (destroyed colloid -> leads to leaking of thyroid hormone)
then progresses to hypothyroidism: dec. T4 and inc. TSH
33
What hormone controls the number of TRH receptors on the anterior pituitary?
T4; less T4 -> more TRH receptors
34
Hashimoto Thyroiditis
| Histology
Germinal Centers!
Chronic Inflammation
Herthle Cell change
35
What do patients with Hashimoto Thyroiditis have an increased risk of developing?
B-cell lymphoma -> present with enlarging thyroid gland with HT
Germinal Centers generate post germinal center B cells -> marginal zones -> marginal zone lymphoma
36
Subacute (deQuervain Granulomatous Thyroiditis)
Cause?
Presentation?
Granulomatous thyroiditis that follows a viral infection
Presents as tender thyroid with transient hyperthyroidism
Self-limited; does not progress to hypothyroidism.
37
Woman has a tender thyroid, what is the first diagnosis to consider?
Subacute (deQuervain Granulomatous Thyroiditis)
38
Reidel Fibrosing Thyroiditis
What is it?
Key "phrase" in a question stem?
Chronic inflammation with extensive flibrosis of thyroid
Presents as hypothyroidism with HARD AS WOOD, NON TENDER THYROID GLAND.
Fibrosis can extend to local areas.
39
Are thyroid nodules likely to be benign or malignant?
Benign
40
What is the key mechanism to sampling the thyroid?
FNA
41
Increased uptake of 131-I is seen it what diseases?
Usually benign conditions, such as Graves or nodular goiter.
42
Decreased uptake of 131-I is seen in what conditions?
It can be benign or malignant.
| Adenoma and carcinoma are decreased uptake.
43
Follicular Adenoma
| Histology
Tumor is making follicles, but there is a dense pink capsule
44
Four types of Thyroid Carcinoma?
Papillary, Follicular, Medullary, Anaplastic
45
Most common type of thyroid carcinoma?
papillary carcinoma
46
Major risk factor for papillary carcinoma?
Exposure to ionizing radiation in childhood.
47
Papillary Carcinoma
| Histology
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)
48
Follicular Carcinoma?
| malignant proliferation of what? How do you differentiate between an adenoma?
Malignant proliferation of follicles
| Surrounded by fibrous capsule with INVASION through capsule.
49
FNA can or cannot distinguish between follicular adenoma and carcinoma?
CANNOT, you need to examine the capsule.
50
How does follicular carcinoma spread?
Hematogenously. Usually carcinomas spread by lymph nodes besides a few, but not this carcinoma.
51
Medullary carcinoma.
Proliferation of what type of cell?
What hormone would you have high levels of?
Malignant proliferation of parafollicular C-cells
| High levels of calcitonin produced by tumor may lead to hypocalcemia.
52
Medullary carcinoma of the thyroid.
| Histology
Calcitonin often deposits within tumor as amyloid (localized amyloidosis).
Malignant tumor cells within amyloid stroma.
53
Familial cases of medullary carcinoma of the thyroid are associated with what mutation?
Often due to MEN 2A and 2B
Associated with mutations in RET oncogene.
Detection of RET mutation warrants prophylactic thyroidectomy.
54
Name the three common MEN 2A neoplasms.
Medullary carcinoma of the thyroid
Pheochromocytoma
Parathyroid Adenomas
55
Name the three categories of common neoplasms associated with MEN 2B.
Medullary carcinoma of the thyroid.
Pheochromocytoma.
Mucosal ganglio-neuromas, particularly of oral mucosa.
56
Aplastic carcinoma of the thyroid?
Description.
Who usually gets it?
Undifferentiated malignant tumor of the thyroid
Usually seen in elderly
Often invades local structures leading to dysphagia or respiratory compromise.
POOR prognosis.
57
How do you differentiate between Reidel Fibrosing Thyroiditis and Aplastic carcinoma of the thyroid?
Reidel is usually seen in younger patients, and aplastic carcinoma is usually seen in the elderly.
58
What is the key cell in the parathyroid gland called? What is it's purpose?
Chief cell
| Regulate serum free (ionized) calcium via PTH secretion
59
What is the most common cause of primary hyperparathyroidism?
Parathyroid adenoma (>80% of cases)
60
What are the consequences of increased PTH and hypercalcemia?
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)
61
Lab findings in hyperparathyroidism?
```
High serum PTH
Low serum P
High serum calcium
Increased urinary cAMP (ATP -> cAMP cascade)
Inc serum Alk Phos
```
62
What is the most common cause of secondary hyperparathyroidism?
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
Lab findings of secondary hyperparathyroidism
High PTH
Low serum calcium
Inc serum phosphate
Inc alkaline phosphatase
64
Hypoparathyroidism causes
Autoimmune damage, surgical excision, DeGeorge syndrome
65
Hypoparathyroidism CP
numbness and tingling
muscle spasms (tetany)
Dec PTH and dec serum Ca
66
Pseudohypoparathyroidism description
Due to end-organ resistance to PTH
| Hypocalcemia with HIGH PTH levels
67
Why do Cushing syndrome patients have moon facies, buffalo hump, truncal obesity?
High glucose -> excess insulin -> storage of fat
68
Why do Cushing syndrome patients have abdominal striae?
Cortisol inhibits the synthesis of collagen -> weak collagen -> blood vessels rupture easily
69
Why do Cushing syndrome patient's have hypertension?
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
Cortisol is used as an immunosuppressant in three major ways. Describe
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
How do you diagnose Cushing syndrome?
increased 24 hr urinary cortisol level
72
What is the most common cause of Cushing syndrome?
Exogenous corticosteroids -> leads to atrophy of BOTH adrenals
73
When comparing the adrenal glands, will they be the same size or different size with a primary adrenal adenoma, hyperplasia or carcinoma?
Different size. One tumor will be excessively secreting cortisol and get larger and the other will atrophy.
74
What will a high-dose dexamethasone test determine?
Dexamethasone will suppress ACTH production by a pituitary adenoma, but will fail to suppress ectopic ACTH production by a small cell lung carcinoma.
75
What happens to Na, K and Hydrogen ion in response to aldosterone?
Sodium is absorbed, K is excreted and Hydrogen ion is excreted.
76
Hyperaldosteronism effects?
Hypernatremia
Hypokalemia
Metabolic Alkalosis
Patient will also have hypertension
77
Most common cause of Primary hyperaldosteronism?
adrenal adenoma
| characterized by high aldosterone and low renin
78
Secondary hyperaldosteronism cause?
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
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?
CAH from 11-hydroxylase deficiency
80
What are signs and symptoms of a 17-hydroxylase deficiency for CAH?
No cortisol or sex steroid production, excess mineralocorticoids.
Always no cortisol, so excess ACTH leading to CAH.
81
Waterhouse-Friderichsen syndrome clinical presentation:
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
"Sack of blood" adrenal gland on gross examination in characteristic of what condition?
Waterhouse-Friderichsen syndrome
83
What are the three major causes of chronic insufficiency of the adrenal glands?
```
Autoimmune destruction -> developed world
TB -> developing world
Metastatic carcinoma (LUNG CANCER LOVES TO GO TO THE ADRENAL)
```
84
Chronic Renal insufficiency clinical features?
Hypotension (cortisol)
Hyponatremia, Hyperkalemia, hypovolemia (aldosterone)
Weakness
Hyperpigmentation (cortisol due to excess ACTH)
Vomiting and Diarrhea (cortisol)
85
ACTH is derived from what molecule?
POMC
| Derivative of POMC is melanocyte stimulating hormone (MSH)
86
Chromaffin cells are derived from what embryologic component? Where are they located? What is their physiologic function?
Neural crest
Adrenal Medulla
Main physiologic source of catecholamines (E and NE)
87
Pheochromocytoma is a tumor of what? Describe the gross and histological presentation.
Chromaffin cells
| Brown Tumor because adrenal medulla is brown
88
Clinical features of a pheochromocytoma?
```
Episodic HTN
Headaches
Palpitations
Tachycardia
Sweating
```
89
How do you diagnose a pheochromocytoma? Treatment?
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
Rules of 10 is referring to what condition? What are they?
```
Pheochromocytoma
10% bilateral
10% familial
10% malignant
10% located outside adrenal medulla (bladder wall)
```
91
What are conditions associated with pheochromocytoma?
MEN2A and 2B
VHL disease
NF type 1
92
What is the classic presentation of Toxic multinodular goiter?
Older adult with history of nontoxic multinodular goiter.
| May have cardiac complications such as a.fib and/or heart failure
93
Thyroiditis is typically caused by what? If tissue inflammation and destruction occurs, what can be the result?
Typically caused by viral infection but broad differential (could also be hashimoto thyroiditis).
Release of preformed thyroid hormone, leading to transient thyrotoxicosis.
94
What does thyrotoxicosis mean?
Excess of thyroid hormone in the body
95
What are potentially permanent causes of thyrotoxicosis?
Graves Disease, Toxic multinodular goiter, Toxic adenoma, pituitary adenoma
96
What are some transient causes of thyrotoxicosis?
```
Hashimoto Thyroiditis
Subacute thyroiditis (de Quervain thyroiditis)
Iodine-induced (jodbasedow effect)
```
97
If a patient has unintentional weight loss with a preserved or increased appetite, what three diagnosis should one consider?
Hyperthyroidism
Diabetes Mellitus
Malabsorption syndrome
98
What is myxedema coma?
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
Differential Diagnosis of Hypothyroidism?
```
Endemic Cretinism (I deficient)
Endemic Goiter (I deficient)
Hashimoto Thyroiditis
Iatrogenic (thyroidectomy)
Riedel thyroiditis (chronic fibrosis)
de Quervain thyroiditis (viral in nature)
```
100
What are two anabolic actions of GH?
Promotes tissue growth of MS system and visceral organs
| Stimulates liver to secrete IGF-1
101
What is acromegaly?
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
What hormone does dopamine inhibit?
Prolactin
103
What are the three metabolic actions of GH?
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
What processes stimulate GHRH release from the hypothalamus?
Fasting, Sleep, Hypoglycemia, Stress!
105
Where is GH secreted and from what type of cell?
Pituitary, somatotroph
106
What hormone inhibits GH release?
Somatostatin
107
Liver IGF inhibits secretion of what hormones?
Feedback inhibition of GHRH and GH
108
What is a growth-hormone suppression test?
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
What will happen if you administer insulin to a patient who is suspected to have GH hyposecretion.
GH will fail to secrete despite the provoked hypoglycemia and is evidence of a pituitary GH hyposecretion or panhypopituitarism, or both.
110
Hyperglycemia inhibits or stimulates GH secretion?
Inhibits.
111
What is octreotide?
Synthetic somatostatin analogue.
| Treats GH-secreting tumors of the anterior pituitary.
112
What does an absence of ADH lead to?
Dilution of urine
| Loss of free water
113
What are some of ADH's physiological actions?
stimulates FREE WATER reabsorption by kidneys (concentrates urine), increases plasma volume, decreases plasma osmolarity
High concentrations, promotes systemic vasoconstriction -> increased arteriole BP
114
What regulates ADH secretion?
Hypothalamic osmoreceptors -> shrink or swell by changing plasma osmolarity
115
What triggers ADH secretion?
Increased plasma osmolarity
| Decreased plasma volume
116
Central DI pathophysiology?
Deficiency of functional ADH
117
Nephrogenic DI pathophysiology?
Tissue insensitivity (collecting tubule) to circulating ADH
118
What is the classic presentation of DI?
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
Will central or peripheral DI respond to administration of synthetic ADH?
Central
120
What is a common cause of nephrogenic DI?
Long term lithium use
121
What are some common causes of Central DI?
Head Trauma
Hypothalamic Lesions
Neoplasms
Gene mutations in vasopressin gene
122
What is another name for ADH?
arginine vasopressin; vasopressin
123
If synthetic ADH is administered to a patient with central DI, what will happen to their urine?
It will become concentrated
124
If a patient has pathological increased levels of ADH, what will happen to the plasma osmolarity?
Plasma osmolarity will be reduced and dilutional hyponatremia will occur.
125
What is the condition in which the patient is always concentrating urine and never diluting urine?
SIADH ( Syndrome of inappropriate antidiuretic hormone secretion)
Urine will be inappropriately concentrated given the low plasma sodium concentration.
126
What are oxytocin's functions?
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
B-cells lie in what portion of the islets?
The center of the islets
128
What receptor is up regulated by insulin in skeletal muscle?
GLUT4 allowing glucose to enter into those tissues
129
What is the pathophysiology of DM Type I?
Autoimmune destruction of B-cells by T lymphocytes
| Inflammation of the islets
130
What MHC Class II cell surface receptors are associated with Diabetes Mellitus Type I?
HLA-DR3 and HLA-DR4
| Can also have autoantibodies against insulin in blood
131
Why will patients have weight loss and low muscle mass in DM Type 1?
The patients have unopposed glucagon --> leading to gluconeogenesis and requiring energy (a.a.) so there will be glycogenolysis, lipolysis and breaking down muscle.
132
How does DKA usually arise?
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
What are the ketone bodies?
B-hydroxybutyric acid, acetoacetic acid, acetone.
134
Clinical features of DKA?
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
Treatment for DKA??
Fluid
Insulin
Replacement of electrolytes (potassium)
136
Besides glucose, insulin also drives what metabolite into cells?
potassium
137
Type II DM Pathophysiology?
End-organ insulin resistance -> metabolic disorder characterized by hyperglycemia.
138
Which has a stronger genetic predisposition, Type 1 or Type 2 DM?
Type 2 Diabetes Mellitus
139
What are histologic features for DM Type II?
Islets will become full of amyloid
140
Describe quantitatively the levels of insulin for a DM Type II patient.
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
Clinical features of DM Type II
Polyuria
Polydipsia
Hyperglycemia
Often clinically silent
142
Treatment for DM Type II?
Weight Loss (Diet and Exercise)
Drug therapy to counter insulin resistance
Insulin in the later stages of the disease.
143
What are DM Type II patients at risk for developing? What is the cause of it?
Hyperosmolar non-ketogenic coma.
High glucose levels (>500 mg/dL) leads to life threatening diuresis
Hypotension and coma
Ketones are absent!
144
What does NEG stand for?
Non enzymatic glycosylation
145
What are some complications from NEG of vascular BM? What patients are at risk?
Diabetes Mellitus Type II!
NEG of large- and medium- sized vessels --> atherosclerosis.
NEG of small vessels -> hyaline arteriolosclerosis
NEG of hemoglobin -> HbA1c
146
What cells can take up sugars without the need for insulin?
Schwann Cells
Pericytes of retinal blood vessels
Lens
147
What enzyme converts glucose to sorbitol?
aldose reductase
148
MEN 1 neoplasms?
Pituitary Adenoma
Pancreatic Endocrine tumor (tumor of islet cells)
Parathyroid hyperplasia
149
Insulinoma lab findings for glucose, insulin and C-peptide
Decrease glucose
Increase insulin
Increase C-peptide
150
What should you consider if a patient has high insulin but not an increase in C-peptide?
Malingering, the patient is injecting insulin into themselves since C-peptide is produced with insulin within the body.
151
Episodic hypoglycemia with mental status changes that are relieved by glucose. Possible Diagnosis to consider?
Insolinoma
