Brainscape's Knowledge GenomeTM

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


See full index

Pathology > Endocrine Pathology > Flashcards

Endocrine Pathology Flashcards

1
Q

Endocrine System
(4)

A
  • Maintain metabolic equilibrium (homeostasis)
  • Secrete chemical messengers (hormones)
  • Regulate activity of various organs
  • Process of feedback inhibition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Process of feedback inhibition

A
  • Increased activity of target tissue, typically down-
    regulates activity of gland secreting stimulating
    hormone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Endocrine diseases
a. diseases of
b. diseases associated with

A

under/over-production of hormones
development of mass
lesions

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

Tumors of endocrine glands, whether benign or
malignant, may secrete the hormone native to the gland. Such
tumors are said to be “—” tumors. It may be the mass effect
of the tumor or the metabolic effect of the excessive hormone that
calls attention to the tumor.

A

functional

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

Endocrinopathies
organs (6)

A
  • Anterior Pituitary
  • Posterior Pituitary
  • Thyroid
  • Parathyroid
  • Pancreas
  • Adrenal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pituitary gland
* Base of brain-

A

sella turcica

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

Pituitary gland
Connected to

A

hypothalamus
a. stalk composed of axons
b. venous plexus

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

Pituitary gland
Central role in regulation of

A

other endocrine
glands

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

Pituitary gland
Two components

A

a. anterior lobe (adenohypophysis)
b. posterior lobe (neurohypophysis)

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

Pituitary gland
Diseases divided according to — mainly
affected

A

lobe

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

Pituitary: Adenohypophysis
(5)

A

Somatotrophs
Lactotrophs
Corticotrophs
Thyrotrophs
Gonadotrophs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  • Somatotrophs
A
  • Produces growth hormone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  • Lactotrophs
A
  • Produces prolactin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  • Corticotrophs
A
  • Produces adrenocorticotrophic hormone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  • Thyrotrophs
A
  • Produces thyroid simulating hormone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  • Gonadotrophs
A
  • Produces follicle stimulating hormone and luteinizing
    hormone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pituitary: Neurohypophysis
(2)

A
  • Antidiuretic hormone
  • (ADH, Vasopressin)
  • Oxytocin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Diseases of anterior pituitary
(2)

A

a. Decreased/increased secretion of trophic
hormones
b. Hypopituitarism/hyperpituitarism

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

Hypopituitarism

A

a. Destructive lesions/processes –ischemia,
radiation, inflammation, neoplasms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Hyperpituitarism
(2)

A

a. Functional adenoma within anterior lobe
b. Local mass effects –enlargement of sella turcica,
visual field abnormalities, increased intracranial
pressure

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

Hypopituitarism
(4)

A
  • Pituitary Adenomas
  • Radiation Treatment
  • Neurosurgery
  • Sheehan Syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Sheehan Syndrome

A
  • Ischemic necrosis of pituitary gland
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Clinical Manifestation:
Hypopituitarism
(6)

A
  • Pituitary Dwarfism
  • Amenorrhea & Infertility
  • decreased Libido & Impotence
  • Postpartum lactation failure
  • Hypothyroidism
  • Hypoadrenalism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Hyperpituitarism
(4)

A
  • Pituitary Adenomas
  • Pituitary Hyperplasia
  • Pituitary Carcinomas
  • Hypothalamic disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Clinical Manifestation:
Hyperpituitarism
(3)

A
  • Gigantism
  • Acromegaly
  • Cushing disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Hyperpituitarism (Gigantism)
(3)

A
  • Primary tumor
  • Excess growth hormone (GH)
  • Affects all “growing tissues”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q
  • Excess growth hormone (GH)
    (2)
A
  • Adenoma of anterior
    pituitary
  • 2nd most common
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q
  • Affects all “growing tissues”
  • Gigantism-
A

before growth
plate closure

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

Gigantism
*Generalized
overgrowth
* — standard deviations

A

3

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

Gigantism
symptoms (6)

A

*Headaches
*Chronic fatigue
*Arthritis,
osteoporosis
* Muscle weakness
*Hypertension
*Congestive heart

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

Acromegaly
(6)

A
  • Late diagnosis
  • Poor vision; photophobia
  • Enlarged skull, hands, feet, ribs
  • Soft tissue, viscera
  • Enlarged maxilla, mandible, nasal and frontal
    bones, maxillary sinus
  • Intraoral:
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Acromegaly
intraoral:
(5)

A
  • Diastemas
  • Malocclusion
  • Macroglossia
  • Enlarged lips
  • Sleep apnea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Posterior Pituitary
(2)

A
  • Diabetes Insipidus (Central)
  • Secretions of Inappropriately High
    Levels of ADH (SIADH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Diabetes Insipidus (Central)
(2)

A
  • Polyuria
  • Dilute urine
  • Polydipsia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Secretions of Inappropriately High
Levels of ADH (SIADH)
(4)

A
  • Hyponatremia
  • Cerebral edema
  • Neurologic dysfuction
  • increase Total Body Water
  • Blood volume normal
  • No peripheral edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

iodine from a normal diet is stored in the

A

thyroid gland (bound to thyroglobulin) and used for T3 and T4 production

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

T3 and T4 difference

A

addition of iodide

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

T3 and T4 production

A

T3: T4 conversion
T4: produced by the thyroid

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

activator for the synthesis of TSH

A

TRH

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

activator for T3/4 production

A

TSH

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

3 glands responsible for the thyroid function

A

hypothalamus
pituitary
thyroid

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

a very small percentage of T3 and T4 is not bound to thyroxine binding proteins and remains

A

free in circulation

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

Hypothyroidism
* Primary
(4)

A
  • Intrinsic abnormality
    in the thyroid
  • Surgery
  • Radiotherapy
  • Autoimmune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Hypothyroidism
* Secondary
(1)

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

Myxedema
(7)

A
  • Adult
  • Generalized fatigue
  • Apathy
  • Mental sluggishness
  • Listless
  • Cold intolerance
  • Overweight
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Cretinism
(6)

A
  • Childhood
  • Impaired skeletal
    development
  • Severe mental
    retardation
  • Short stature
  • Course facial features
  • Delayed tooth
    eruption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

symptoms of hypothyroidism
(5)

A

cold intolerance
fatigue, lethargy
weight gain
constipation
bradycardia

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

Hypothyroidism
* Diagnosis
(2)
* Treatment
(1)

A
  • TSH
  • Increased (Primary)
    -Decreased (Secondary)
  • T4 low
  • Supplement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Hashimoto Thyroiditis
(4)

A
  • Autoimmune
  • Painless
    enlargement
  • Symmetric &
    diffuse
  • Risk of B-cell non-
    Hodgkins
    Lymphomas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

ETIOLOGICAL AND CLINICAL ASPECTS
OF HYPERTHYROIDISM
Clinical signs and symptoms
(7)

A

Goiter (small)
Exophtalmus (frequent)
Heat intolerance
Weight loss
Malabsorption and diarrhea
Tachycardia
Irritability and anxiety

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

ETIOLOGICAL AND CLINICAL ASPECTS
OF HYPERTHYROIDISM
Most common causes
(2)

A

Autoimmune - Graves’ disease and
Hashimoto’s thyroiditis

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

ETIOLOGICAL AND CLINICAL ASPECTS
OF HYPERTHYROIDISM
Laboratory
(3)

A

T4 and Free T4 elevated
T3 and Free T3 elevated
TSH and TRH suppressed

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

symptoms of hyperthyroidism
(5)

A

weight loss
nervousness
rapid pulse
goiter
muscle wasting

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

hyperthyroidism

A

despite low TSH levels, the thyroid continues to produce elevated t3/4 levels. this is possible bc of the autoantibodies which stimulate the thyroid hormone production. this hyperfunction is permanent

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

Hyperthyroidism
Graves Disease
(5)

A
  • Tachycardia
  • Increased appetite
  • Weight loss
  • Exophthalmos
  • Intolerance to heat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Hyperthyroidism
Graves Disease
* Diagnosis
(2)

A
  • TSH
  • Primary-low
  • Secondary- normal to high
  • T4 (T3) increased
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Hyperthyroidism
Graves Disease
Treatment

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

Hyperthyroidism
Graves Disease
* Significance
(5)

A
  • Thyroid storm
  • Caused by infection, stress,
    trauma
  • Elevated body temp.
  • Tachycardia
  • 20-40% mortality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Diffuse & Multinodular Goiter
(4)

A
  • Thyroid enlargement
  • Impaired synthesis of thyroid
    hormone
  • Maintenance of minimal function
    (euthyroid)
  • Diffuse early on, then nodular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q
  • Impaired synthesis of thyroid
    hormone
    (2)
A
  • Iodine deficiency
  • Endemic
  • Hyperplasia of follicles
  • Pituitary stimulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Sequence Of Events In Endemic Goiter
(4)

A
  • Diet deficient in iodine
  • Decreased output of T3 & T4 by thyroid
  • Pituitary responds by secreting TSH
  • Thyroid hyperplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Thyroid Neoplasms
* Adenoma
(4)

A
  • Solitary
  • Males
  • Younger
  • Warm/Cold nodules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Thyroid Neoplasms
* Papillary Carcinoma
(5)

A
  • 75-85%
  • All ages
  • Radiation
  • 10 yr = 95%
  • Worse in elderly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Thyroid Neoplasms
* Follicular Carcinoma
(4)

A
  • 10-20%
  • Older
  • Iodine deficiency
  • Cold nodules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Thyroid Neoplasms
* Medullary Carcinoma
(5)

A
  • 5%
  • Neuroendocrine
  • Calcitonin (C cells)
  • Amyloid
  • MEN 2 A/B (20%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

PARATHYROID GLANDS
(4)

A

Derived from developing pharyngeal pouches
Lie in close proximity to upper and lower poles of each thyroid
lobe
May be found on path of descent of pharyngeal pouches –
carotid sheath, thymus, anterior mediastinum
Secrete Parathormone (PTH) which, with calcitonin regulates
calcium homeostasis –controlled by the level of free (ionized)
calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

PTH:
(5)

A

Activates osteoclasts activity
Increases Ca renal tubular resorption
Increases conversion of Vit. D into the active
dihydroxy form in the kidneys
Increases urinary excretion of phosphates
Increases Ca absorption by the GI tract.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Hypoparathyroidism
(3)

A

*Surgically induced
- Iatrogenic
*Congenital absence
- DiGeorge Syndrome
*Autoimmune
- APECED

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Hypoparathyroidism
(3)

A

Hypocalcemia
Chvostek Sign
Trosseau sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

*Hypocalcemia

A

*Tetany

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

*Chvostek Sign

A

*Tapping CN VII
- Muscle contraction
- Eye, mouth, nose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

*Trosseau sign

A

*Occluding circulation of forearm
- Carpal spasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Hyperparathyroid Pathology
* Primary
(3)

A
  • Adenoma (75-80%)
  • One gland
  • Hyperplasia (10-15%)
  • Multiglandular
  • MEN 1 & 2a,b
  • Carcinoma (<5%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Hyperparathyroid Pathology
* Secondary

A
  • Renal failure
  • Hyperphosphatemia
  • Chronic hypocalcemia
  • Vitamin D deficient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

PRIMARY
HYPERPARATHYROIDISM
(4)

A

Adenoma
Hyperplasia
Carcinoma
Serum calcium levels, especially Ionized calcium levels are high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

PRIMARY
HYPERPARATHYROIDISM
Morphologic changes
(5)

A

Skeletal changes - bone resorption
- Formation of bone cysts and hemorrhages
(osteitis fibroso –cystica) - Brown tumors
-Urinary tract stones (nephrolithiasis)
- Metastatic calcification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Primary Hyperparathyroidism
(3)

A

*Hypercalcemia
* Hypophosphatemia
* Increased urinary excretion of both calcium and
phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

SECONDARY HYPERPARATHYROIDISM
(2)

A

Calcium is chronically depressed and low serum calcium
levels lead to compensatory hyperactivity of the
parathyroids
Serum phosphate levels are elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

SECONDARY HYPERPARATHYROIDISM
Causes
(4)

A

Chronic renal failure
Vitamin D deficiency
Inadequate dietary calcium
Steatorrhea

80
Q

SECONDARY HYPERPARATHYROIDISM
Morphology
(3)

A

Hyperplastic parathyroid glands
Bone chages (see primary hyperparathyroidism)
Metastatic calcification

81
Q

SECONDARY HYPERPARATHYROIDISM
Clinical features
(5)

A

Not as severe as in primary hyperparathyroidism
Related to symptoms secondary to chronic renal failure
Bone abnormalities (renal osteodystrophy)
Calciphylaxis
Tertiary hyperparathyroidism

82
Q

Hyperparathyroidism
(5)

A
  • Osteomalacia & loss of lamina dura
  • Brown tumor
  • Nephrolithiasis
  • Peptic/duodenal ulcers
  • Mental changes
83
Q

PTH Actions
(6)

A
  • Increases serum calcium
  • Activates osteoclasts
  • Increases renal tubular reabsorption of
    calcium
  • Increases renal conversion of Vit D
  • Increases urinary excretion of phosphate
  • Increased gastric absorption of calcium
84
Q

Zona Glomerulosa
(2)

A
  • Aldosterone
  • Regulated by angiotensin II
85
Q

Zona Fasiculata
(2)

A
  • Glucocorticoids (cortisol)
  • Regulated by ACTH (biofeedback)
86
Q

Zona Reticularis
(2)

A
  • Androgens
  • No feedback with ACTH
87
Q

Adrenal Cortex Pathology
Too Little
(3)

A
  • Adrenal insufficiency
  • Acute
  • Waterhouse-Friderichsen
  • Primary Chronic
  • Addison Disease
  • Secondary
88
Q

Adrenal Cortex Pathology
Too Much
(3)

A
  • Hyperaldosterism
  • Hypercorticolism
    – Cushing Syndrome
  • Adrenogenital syndrome
89
Q

Hypoadrenocorticism
Addison’s Disease
(11)

A
  • Destruction of adrenal cortex
  • decreased Production of adrenal corticosteroid hormones
  • Autoimmune
  • Metastatic carcinoma
  • Infections, TB, AIDS
  • Deep fungal
  • Secondary hypoadrenocorticism
  • Disorder of hypothalamus or pituitary gland
  • Clinical symptoms appear late
  • Weakness & Fatigue
  • Hypotension (postural)
  • GI disturbances
  • Hyper-pigmentation (Bronzing)
  • ACTH precursor stimulates melanocytes
  • Frictional areas
  • Adrenal Crisis (Acute
90
Q
  • GI disturbances
    (5)
A
  • Nausea/ Vomiting (N/V)
  • Anorexia
  • Diarrhea
  • Weight Loss
  • Salt cravings ( K+ ↑, Na+↓,)
91
Q
  • Hyper-pigmentation (Bronzing)
    (2)
A
  • ACTH precursor stimulates melanocytes
  • Frictional areas
92
Q
  • Adrenal Crisis (Acute)
    (3)
A
  • Abdominal pain
  • Hypotension
  • Vascular collapse
93
Q

Hypercortisolism
*Primary
(6)

A
  • Too much endogenous steroid
  • Females 5x
  • 3rd decade
  • Pituitary adenomas (ACTH)
  • 50%
  • Cushing disease
  • Adrenal hyper/neoplasia
  • 10-20%
  • Neuroendocrine tumors
  • Produce ACTH
  • Small Cell Lung Carcinoma
94
Q

Hypercortisolism
*Secondary
(4)

A
  • Most common
  • Exogenous
  • Rule of 2s
  • Can become hypocortisol
    without taper
95
Q

Hypercortisolism
(Cushing syndrome)
(11)

A
  • Presentation
  • Central obesity
  • Peripheral wasting
  • Buffalo hump
  • “Moon facies”
  • Abdominal striae
  • Hirsutism
  • Poor wound healing
  • Diabetes
  • Hyperglycemia
  • Osteoporosis
  • Hypertension
96
Q

Adrenal Neoplasms
Cortex
* Adenomas
(3)

A
  • Cushing
  • Hyperaldosteronism
  • “Incidentalomas”
97
Q

Adrenal Neoplasms
* Carcinomas
(3)

A
  • Rare
  • Virilizing adenoma
  • Li-Fraumeni & Beckwith-
    Wiedemann
98
Q

Adrenal Neoplasms
Medulla
(3)

A
  • Pheochromocytoma
  • Neuroblastoma
  • 10% tumor
  • 10% Familial (MEN 2A,B)
  • 10% extra-adrenal
  • 10% are bilateral
  • 10% are malignant
99
Q
  • MEN 1- AD; Chr 11q (TSG)
    (3)
A
  • Pancreas (95%): insulinomas, gastrinomas
  • Parathyroid (40%): hyperplasia
  • Pituitary (30%): Prolactinomas
100
Q
  • MEN 2A- AD; Chr10q (RET proto-onco gene)
    (1)
A
  • Adrenal Medulla (50%); Med.Thy.Ca.; PT- hyperplasia
101
Q
  • MEN 2B
    (1)
A
  • MEN 2A + marfanoid habitus; mucosal neuromas
102
Q

MEN 2B
(5)

A
  • AD
  • Marfanoid body type
  • Medullary thyroid carcinoma
  • Pheochromocytomas
  • Neuromas
103
Q
  • Pheochromocytomas
    (1)
A
  • Adrenal medulla
104
Q
  • Neuromas
    (4)
A
  • Can be first sign
  • Soft painless papules
  • Lips, conjunctiva, tongue,
    palate, buccal mucosa
  • Sentinel neuromas
105
Q

Pancreas
* Exocrine Pancreas
(4)

A
  • Secretes enzymes
  • Digestion
  • Inactive proenzymes
  • Acute pancreatitis
  • Chronic pancreatitis
  • Cancer
106
Q

Pancreas
* Endocrine Pancreas
(3)

A
  • Secretes hormones
  • Glucose homeostasis
  • Other metabolic activities
  • Diabetes mellitus
  • Beta cells in the islets of
    Langerhans
107
Q

Acute Pancreatitis
(3)

A
  • Injury to acinar cells
  • Interstitial or edematous pancreatitis
  • Mild, Reversible
  • Acute hemorrhagic pancreatitis
  • Alcoholism, Chronic biliary disease
108
Q

Acute Pancreatitis Etiology
* Metabolic
(5)

A
  • Alcoholism
  • Hyperlipoproteineimia
  • Hypercalcemia
  • Drugs- Thiazide diuretics
  • Genetic
109
Q

Acute Pancreatitis Etiology
* Mechanical
(3)

A
  • Trauma
  • Gallstones
  • Iatrogenic injury
  • Perioperative injury
  • Endoscopic procedures with dye injections
110
Q

Acute Pancreatitis Etiology
* Vascular
(3)

A
  • Shock
  • Atheroembolism
  • Polyarteritis nodosa
111
Q

Acute Pancreatitis Etiology
* Infectious
(3)

A
  • Mumps
  • Cocksackievirus
  • Mycoplasma pneumoniae
112
Q

Chronic Pancreatitis
(5)

A
  • Destruction of pancreatic parenchyma
  • Intermittent “acute” attacks
  • Alcoholism
  • Obstruction of pancreatic duct
  • Chronic injury to acinar cells
113
Q
  • Obstruction of pancreatic duct
    (4)
A
  • Mechanical blockage
  • Congenital defects
  • Cancer
  • Inspissated mucous
114
Q

Exocrine Pancreatic
Neoplasms
(3)

A
  • Pancreatic cystic neoplasm
  • Pancreatic cancer
  • Acinar cell carcinoma
115
Q

Endocrine Pancreatic
Neoplasms
* Islet cell tumors
(2)

A
  • Insulinoma
  • Glucagonoma
  • Mild diabetes
  • Rash
116
Q

Endocrine Pancreatic
Neoplasms
* Pancreatic Gastrinoma

A
  • Zollinger-Ellison Syndrome
  • Hypersecretion of gastric acid
  • Peptic ulcers
  • High blood gastrin
117
Q

is diabetes a single disease

A

no

118
Q

Endocrine Pancreas
* Islets of Langerhans
* Alpha cells –
* Beta cells –

A

glucagon
insulin - diabetes mellitus

119
Q

Diabetes Mellitus
(3)

A
  • Hyperglycemia
  • 21 million people ( 7% of population)
  • Loss of insulin (anabolic) results in a catabolic state
    affecting glucose, fat & protein metabolism
120
Q
  • Hyperglycemia
    (3)
A
  • Lack of insulin (Type 1)
  • Resistance to insulin (Type 2)
  • Combination
121
Q

Type 1 Diabetes Mellitus
Archaic terminology:
def:

A
  • Insulin Dependent DM, juvenile-onset DM
  • Autoimmune destruction of B cells in the Islets of Langerhans (insulitis)
122
Q

Diabetes Mellitus
* Type 1
(6)

A
  • Absolute deficiency
  • Destruction of Beta cells
  • Only 10% diabetics
  • Avg. age of onset- 14 yo
  • Emergencies
    Slow progression despite
    abrupt clinical onset
123
Q
  • Emergencies
  • Acute:
  • Chronic:
A

hypoglycemia
ketoacidosis

124
Q

Type 1 Diabetes Mellitus
*Cause-
* Autoimmune
(2)
* Genetic
(2)
* Environmental?
(1)

A
  • Destruction of β-cells
  • T cell mediated
  • Auto-antibodies
  • 30-70% twin concordance
  • HLA-DR3, DR4 (90-95%)
  • Infectious
125
Q

Type 1 Diabetes Mellitus
*Diagnosis ( DM1 or 2)
(4)

A
  • WNL= 70-120 mg/dL
  • Any of these
  • ≥ 200 mg/dL + S/S
  • Fasting ≥ 126 mg/dL
  • OGTT ≥ 200 mg/dl (2 hrs)
126
Q

Pathogenesis of Type 1
Diabetes Mellitus
* Genetic factors
* Autoimmunity
* Environmental factors
*(2)

A
  • Viruses- Coxsackie B
  • Chemicals
127
Q

Diagnosis of
Diabetes Mellitus
(2)

A
  • Fasting venous plasma glucose of >140 mg/dl on more than
    one occasion
  • Following ingestion of 75 grams of glucose
128
Q
  • Following ingestion of 75 grams of glucose
    (2)
A
  • 2hr venous plasma glucose concentration >200 mg/dl
  • At least one glucose value during that period is >200 mg/dl
129
Q

Diabetes Mellitus Type 2
* Adult onset
(5)

A
  • “Relative” lack of insulin
  • 80-90% of diabetics
  • Insulin resistance
  • Demographics are changing
  • Ketoacidosis (rare)
130
Q
  • Insulin resistance
    (3)
A
  • Early Normal blood insulin level
  • Target tissue Resistance
  • β-cell dysfunction fails to
    compensate
131
Q
  • Ketoacidosis (rare)
A
  • Coma due to hyperosmolarity
132
Q

Type 2 Diabetes Mellitus
* Archaic terminology:
* Inadequate secretion of — from the pancreas
* Reduced tissue sensitivity to —
* Initially,
* Eventually,

A

Non-Insulin dependent DM, adult/maturity-onset DM
insulin
insulin (liver, skeletal muscle, adipose tissue)
hyperinsulinemia may compensate for peripheral insulin resistance
and normal plasma glucose is maintained
B cell compensation becomes inadequate and there is progression
to hyperglycemia

133
Q

Diabetes Mellitus Type 2
*Obesity
*Genetics
(3)

A

*50-90% of twins
*20-40% of 1st degree
* Only 5-7% in population

134
Q

Pathogenesis of Type 2
Diabetes Mellitus
* Genetic factors
(3)
* Glucose metabolism
* Beta cell function
(1)

A
  • Familial history
  • Obesity
  • Hypertension
  • Impaired release of insulin in response to glucose stimulation
135
Q

DM Type 2
Clinical Progression
(6)

A
  • Only after 90% destruction of the 106 β-cells
  • Polyuria
  • Polydypsia
  • Polyphagia
  • Fatigue/wasting
  • Ketosis (chronic)
136
Q
  • Ketosis (chronic)
    (3)
A
  • Ketone bodies (alternative energy source)
  • Ketoacidosis & diabetic coma= DM1
  • Hyperosmolar non-ketotic coma= DM2
137
Q

Glycosylated Hemoglobin
(Hb A1C) (Glycohemoglobin)
(2)

A
  • The fraction of glycosylated hemoglobin
    in circulating red blood cells
  • Reflects the degree of hyperglycemia
    during the preceding 6-8 weeks
138
Q

Pathogenesis of the
Complications of Diabetes
* Macrovascular disease –
* Microvascular disease –

A

large and medium-sized arteries
capillary dysfunction in target organs

139
Q

Macrovascular Disease –
(3)

A
  • Heart - myocardial infarction
  • Brain - stroke
  • Peripheral vascular disease –lower extremity
    gangrene
140
Q

Microvascular Disease
(3)

A
  • Retina –diabetic retinopathy
  • Kidneys –nephropathy
  • Peripheral nerves - neuropathy
141
Q

Morphology of Diabetes and
Late Complications
* Great variability among patients in
(4)

A
  • Time of onset
  • Severity
  • Organs involved
  • Tight glycemic control delays onset
142
Q

In most patients, changes are likely to be found in:
(5)

A
  • Arteries (macrovascular changes)
  • Basement membrane of small vessels (microangiopathy)
  • Kidneys (diabetic nephropathy)
  • Retina (diabetic retinopathy)
  • Nerves (diabetic neuropathy)
143
Q

Late complications
(3)

A
  • Macrovascular disease
  • Atherosclerosis
  • MI is most common cause of death
  • Gangrene of lower extremities
  • Hyaline artiolosclerosis
  • Kidneys
  • Hypertension
  • Microangiopathy
  • Thickened Basement membranes (but still leaky)
  • Nephropathy, Retinopathy, Neuropathy,
144
Q

Acanthosis Nigricans
definition
may be associated with (2)

A
  • A dermatosis characterized by velvety,
    papillomatous, brownish-black,
    hyperkeratotic plaques, typically of the
    intertriginous surfaces and neck
  • May be associated with insulin resistance
    (cutaneous marker for type 2 diabetes)
  • May be associated with internal malignancy
145
Q

Diabetes Mellitus
* Oral Complications
(5)

A
  • Infections- Candida sp., Mucormycosis, Bacterial
  • Slow healing
  • Gingiva- enlargement, erythema
  • Subjective xerostomia
  • Parotid gland enlargement
146
Q

Liver
* Regenerative
(4)

A
  • Remove 60%
  • Minimal change in function
  • 4-6 weeks for almost total
    regeneration of mass
  • The key is the hepatic reticulum
  • Type 4 collagen
  • Fibrosis= Types 1 & 3 collagen
147
Q

Liver
Functions
(6)

A

Metabolic
Synthetic- plasma proteins
Storage
Degrades/Detoxifies
Exocrine
Endocrine

148
Q

Metabolic
(1)

A
  • Glucose homeostasis
149
Q
  • Synthetic- plasma proteins
    (1)
A
  • Albumin, VLDL, LDL, PT,
    Fibrinogen
150
Q
  • Storage
    (4)
A
  • Glycogen
  • Triglycerides
  • Iron, Copper
  • Vitamins- A, D, K
151
Q

Degrades/Detoxifies
* Phase 1 —
(2)
* Phase 2 —
(1)

A

oxidation
* -OH, -COOH
* Cytochrome p450

152
Q

Degrades/Detoxifies
* Phase 1 —
(2)
* Phase 2 —
(1)

A

oxidation
* -OH, -COOH
* Cytochrome p450

conjugation
* Glucuronic acid= Soluble

153
Q

Exocrine
(1)

A
  • Bile (1L/d)
154
Q

Endocrine
(4)

A
  • D3 to 25-hydroxy-cholecalciferol
  • T4 to T3 (active)
  • GHRH
  • Insulin & glucagon degradation
155
Q

Causes of Cirrhosis
(7)

A
  • One of top 10 causes of death
  • ETOH
  • Infection (HBV, HCV)
  • Biliary disease
  • Iron overload (Hemochromatosis)
  • Autoimmune hepatitis
  • 10% idiopathic
156
Q

Cirrhosis Characteristics
(4)

A
  • Diffuse fibrosis and conversion of normal architecture into
    abnormal nodules
  • Bridging fibrosis
  • Parenchymal nodules
  • Micro (3mm);Macro
  • regeneration
  • Entire liver architecture effaced
157
Q

Complications of Cirrhosis
(3)

A
  • LOF
  • Portal hypertension
  • HCCa
158
Q

Loss of Function
(2)

A
  • Hepatocyte death
  • Loss of Microvilli
  • Changes in blood flow
  • Proteins
159
Q

Complications of Cirrhosis
* Portal Hypertension
(6)

A
  • Loss of Type 4 collagen
  • Loss of fenestrated sinusoids
  • Low to high pressure
  • Pressure on central veins due to fibrosis
  • Ascites
  • Portosystemic venous shunts
  • Varices
  • Splenomegaly
160
Q

Portal Hypertension
Clinical Consequences
(4)

A
  • Ascites
  • Formation of portosystemic venous shunts
  • Congestive splenomegaly
  • Hepatic encephalopathy
161
Q

Complications of Cirrhosis
* Ascities
(2)

A
  • Fluid in the peritoneum (500mL)
  • Serous fluid
162
Q

Complications of Cirrhosis
* Pathogenesis
(5)

A
  • Alteration of Starling Forces in the
    sinusoids
  • Fluid is forced into Space of Disse
  • Enhanced by hyoalbuminemia
  • Enhanced hepatic lymphatic drainage
  • Overwhelms capacity of thoracic duct
    drainage
163
Q

Signs & Symptoms of Liver Failure
(6)

A
  • Jaundice
  • Hypoalbuminemia
  • Hyperammonemia
  • NH3 to urea
  • Hypoglycemia
  • Estrogen metabolism
  • Palmar erythema
  • Spider angioma
  • Hypogonadism
  • Gynecomastia
  • Coagulopathy
164
Q

Jaundice is not a disease
(4)

A
  • NON-SPECIFIC sign of liver dysfunction
  • Retention of bile (>2.0 mg/dL)
  • Hepatitis
  • Obstruction (cirrhosis)- Accumulation of conjugated bilirubin
  • Hemolytic anemias
  • Accumulation of un-conjugated bilirubin
  • Cholestasis (Lack of flow of bile)
  • Retention due to obstruction or hepatocyte dysfunction
  • Serum Alk Phos elevated
    231
165
Q

Causes of Liver Disease
(6)

A
  • Alcohol related
  • Drug related
  • Infectious (HCV)
  • Metabolic
  • Neoplasms
  • Autoimmune
166
Q

Alcoholic Liver Disease
(3)

A
  • ETOH causes 60% of Chronic Liver Disease
  • ETOH accounts for 40-50% of deaths due to cirrhosis
  • 5th leading cause of death
167
Q

Forms of liver disease
(3)

A
  • Hepatitic steatosis
  • Alcoholic hepatitis
  • Cirrhossis
168
Q

Drug-induced Liver Disease
(2)

A
  • Predictable(intrinsic)
  • Unpredictable(idiosyncratic)
  • Toxicity + immune reaction
169
Q

Hepatocellular Damage

A
  • Tetracycline
  • Anti-neoplastic agents
  • Mushroom toxins
  • Amanita Phalloides
  • Carbon tetrachloride
  • ETOH
  • Microvesicular fatty change
  • Macrovesicular fatty change
  • Fibrosis/cirrhossis
  • Diffuse/massive necrosis
  • Centrilobular necrosis
  • Macrovesicular fatty change
  • Fibrosis/cirrhossis
170
Q

Drug-induced Liver Disease
* Drug induced chronic hepatitis is
indistinguishable from other causes
(3)

A
  • Alcoholic liver disease
  • Viral Hepatitis
  • Need serology to r/o viral
171
Q

HAV
(6)

A
  • Self limiting
  • No carrier state
  • Life long immunity
  • Vaccine
  • Epidemics
  • Rare fatalities (0.1%)
172
Q

HBV
(5)

A
  • Prolonged incubation
  • Chronic carrier state
  • Increased risk of HCCa
  • Vaccine- Anti-HBs
  • 2 Billion alive today will be
    infected
173
Q

HCV
(5)

A
  • Similar to HBV, but…
  • More cirrhosis risk
  • Used to be transfusion
    related
  • IV drug related
  • Early Tx hopeful for cure
174
Q

HDV
(3)

A
  • Needs HBV (HBsAg)
  • Coinfection of B & D at same
    time
  • low chance
  • Super-infection of a carrier of
    HBV that gets a new HDV
  • More likely
175
Q

Hemochromatosis
(5)

A
  • Excessive accumulation of Iron
  • WNL= 2-6 gms (only 0.5gm in liver)
  • Males 5-7:1 ( earlier than females)
  • 5th-6th decades
  • Iron deposition in liver, pancreas, myocardium,
    skin, joints
176
Q

Hereditary hemochromatosis
(5)

A
  • AR most common
  • HFE gene on Chr 6p
  • Regulation of intestinal absorption is lost
  • Net gain/year of 0.5-1.0 gm
177
Q

Acquired hemochromatosis
(2)

A
  • Known source of excess iron
  • Hemolytic anemia associated with ineffective erythropoiesis
178
Q

Pancreatic fibrosis
(1)

A
  • DM
179
Q

Hemochromatosis
types (5)

A

Hereditary hemochromatosis
Acquired hemochromatosis
Hepatomegaly/dysfunction/Cirrhosis
Pancreatic fibrosis
Skin pigmentation

180
Q

Wilson

A
  • AR disorder of Copper metabolism
  • Chr 13
  • 1:30,000
  • Accumulation in Liver, brain, & eye
  • Normal uptake but:
  • Failure to enter circulation as ceruloplasmin
  • Inability to be excreted in bile
  • Unbound copper spills into circulation
  • Hemolysis
181
Q

Wilson
* Diagnosis

A
  • Onset prior to age 6
  • Elevated hepatic copper, low serum ceruloplasmin, high urinary
    copper
  • Acute/Chronic hepatitis
  • Neuropsychiatric
  • Behavioral changes
  • Parkinson-like
  • Pychosis
  • Kayser-Fleischer rings
182
Q

Reye Syndrome
(4)

A
  • Fatty liver changes & encephalopathy in Kids (<4 yo)
  • Associated with viral infection
  • Begins as pernicious vomiting 3-5 days s/p virus
  • Lethargy, irritability, hepatomegaly
  • Mitochondrial hepatopathy (LOF)
  • ASA association?
183
Q

Neoplasms
Benign

A
  • Nodular hyperplasia
  • Vascular injury
  • Regenerative nodules
  • Cavernous Hemangioma
  • Adenoma
  • Females, BCPs
  • Rupture is a risk
184
Q

Neoplasms
Malignant
* Metastasis-

A
  • Most common neoplasm IN the liver
  • Colon
  • Lung
  • Breast
185
Q

Neoplasms
Hepatocellular carcinoma
(2)

A
  • Most common neoplasm OF the liver
  • Cirrhosis precedes (risk factor)
186
Q

Hepatocellular Carcinoma
(Hepatoma)

A
  • Geographic distributions
  • Asia, Africa
  • 20-40 yo
  • 50% w/o cirrhosis
  • West much lower (8-30x less)
  • Seldom before 60 yo
  • 90% w/ cirrhosis
  • Cirrhosis (alcoholic)
  • HBV (200x), HCV
  • Aflatoxin (Aspergillus flavus)
187
Q

Gallbladder

A
  • Located in the upper right quadrant
  • Stores bile
  • 50mL
  • Releases bile
  • Fat digestion
188
Q

Gallbladder Anatomy

A
  • Lacks muscularis mucosae
  • Submucosa
  • Mucosal lining
  • Fibromuscular layer
  • Subserosal fat
  • Peritoneal covering
189
Q

Gallbladder Disorders
(3)

A
  • Cholelithiasis
  • Cholecystitis
  • Tumors
190
Q

Cholelithiasis

A
  • Cholesterol stones
  • Crystalline cholesterol monohydrate
  • Pigment stones
  • Bilirubin Calcium salts
191
Q

Pathogenesis of Cholesterol Stones
(4)

A
  • Supersaturated bile with cholesterol
  • Gallbladder hypomotility
  • Accelerated cholesterol nucleation
  • Crystals trapped by gallbladder mucous hypersecretions
192
Q

Pathogenesis of Pigment Stones

A
  • Mixture of abnormal insoluble calcium salts of unconjugated
    bilirubin and inorganic calcium salts
193
Q

Cholecystitis
* Acute
(3)

A
  • Acute inflammation
  • Obstruction of the neck or cystic duct
  • Absence of gallstones
194
Q

Cholecystitis
* Chronic
(3)

A
  • Sequel to repeated bouts of acute cholecystitis
  • Absence of acute cholecystitis
  • Gallstones
195
Q

Tumors
(2)

A
  • Carcinoma of the gallbladder
  • Carcinoma of the extrahepatic bile ducts

Pathology (23 decks)

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