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Endocrine Pathology Flashcards

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1
Q

Endocrine System
(4)

A
  • Maintain metabolic equilibrium (homeostasis)
  • Secrete chemical messengers (hormones)
  • Regulate activity of various organs
  • Process of feedback inhibition
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2
Q

Process of feedback inhibition

A
  • Increased activity of target tissue, typically down-
    regulates activity of gland secreting stimulating
    hormone
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3
Q

Endocrine diseases
a. diseases of
b. diseases associated with

A

under/over-production of hormones
development of mass
lesions

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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

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5
Q

Endocrinopathies
organs (6)

A
  • Anterior Pituitary
  • Posterior Pituitary
  • Thyroid
  • Parathyroid
  • Pancreas
  • Adrenal
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6
Q

Pituitary gland
* Base of brain-

A

sella turcica

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7
Q

Pituitary gland
Connected to

A

hypothalamus
a. stalk composed of axons
b. venous plexus

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8
Q

Pituitary gland
Central role in regulation of

A

other endocrine
glands

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9
Q

Pituitary gland
Two components

A

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

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10
Q

Pituitary gland
Diseases divided according to — mainly
affected

A

lobe

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11
Q

Pituitary: Adenohypophysis
(5)

A

Somatotrophs
Lactotrophs
Corticotrophs
Thyrotrophs
Gonadotrophs

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12
Q
  • Somatotrophs
A
  • Produces growth hormone
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13
Q
  • Lactotrophs
A
  • Produces prolactin
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14
Q
  • Corticotrophs
A
  • Produces adrenocorticotrophic hormone
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15
Q
  • Thyrotrophs
A
  • Produces thyroid simulating hormone
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16
Q
  • Gonadotrophs
A
  • Produces follicle stimulating hormone and luteinizing
    hormone
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17
Q

Pituitary: Neurohypophysis
(2)

A
  • Antidiuretic hormone
  • (ADH, Vasopressin)
  • Oxytocin
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18
Q

Diseases of anterior pituitary
(2)

A

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

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19
Q

Hypopituitarism

A

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

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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

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21
Q

Hypopituitarism
(4)

A
  • Pituitary Adenomas
  • Radiation Treatment
  • Neurosurgery
  • Sheehan Syndrome
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22
Q

Sheehan Syndrome

A
  • Ischemic necrosis of pituitary gland
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23
Q

Clinical Manifestation:
Hypopituitarism
(6)

A
  • Pituitary Dwarfism
  • Amenorrhea & Infertility
  • decreased Libido & Impotence
  • Postpartum lactation failure
  • Hypothyroidism
  • Hypoadrenalism
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24
Q

Hyperpituitarism
(4)

A
  • Pituitary Adenomas
  • Pituitary Hyperplasia
  • Pituitary Carcinomas
  • Hypothalamic disorders
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25
Clinical Manifestation: Hyperpituitarism (3)
* Gigantism * Acromegaly * Cushing disease
26
Hyperpituitarism (Gigantism) (3)
* Primary tumor * Excess growth hormone (GH) * Affects all “growing tissues”
27
* Excess growth hormone (GH) (2)
* Adenoma of anterior pituitary * 2nd most common
28
* Affects all “growing tissues” * Gigantism-
before growth plate closure
29
Gigantism *Generalized overgrowth * --- standard deviations
3
30
Gigantism symptoms (6)
*Headaches *Chronic fatigue *Arthritis, osteoporosis * Muscle weakness *Hypertension *Congestive heart
31
Acromegaly (6)
* Late diagnosis * Poor vision; photophobia * Enlarged skull, hands, feet, ribs * Soft tissue, viscera * Enlarged maxilla, mandible, nasal and frontal bones, maxillary sinus * Intraoral:
32
Acromegaly intraoral: (5)
* Diastemas * Malocclusion * Macroglossia * Enlarged lips * Sleep apnea
33
Posterior Pituitary (2)
* Diabetes Insipidus (Central) * Secretions of Inappropriately High Levels of ADH (SIADH)
34
Diabetes Insipidus (Central) (2)
* Polyuria - Dilute urine * Polydipsia
35
Secretions of Inappropriately High Levels of ADH (SIADH) (4)
* Hyponatremia * Cerebral edema * Neurologic dysfuction * increase Total Body Water - Blood volume normal - No peripheral edema
36
iodine from a normal diet is stored in the
thyroid gland (bound to thyroglobulin) and used for T3 and T4 production
37
T3 and T4 difference
addition of iodide
38
T3 and T4 production
T3: T4 conversion T4: produced by the thyroid
39
activator for the synthesis of TSH
TRH
40
activator for T3/4 production
TSH
41
3 glands responsible for the thyroid function
hypothalamus pituitary thyroid
42
a very small percentage of T3 and T4 is not bound to thyroxine binding proteins and remains
free in circulation
43
Hypothyroidism * Primary (4)
* Intrinsic abnormality in the thyroid * Surgery * Radiotherapy * Autoimmune
44
Hypothyroidism * Secondary (1)
* Pituitary failure
45
Myxedema (7)
* Adult * Generalized fatigue * Apathy * Mental sluggishness * Listless * Cold intolerance * Overweight
46
Cretinism (6)
* Childhood * Impaired skeletal development * Severe mental retardation * Short stature * Course facial features * Delayed tooth eruption
47
symptoms of hypothyroidism (5)
cold intolerance fatigue, lethargy weight gain constipation bradycardia
48
Hypothyroidism * Diagnosis (2) * Treatment (1)
* TSH - Increased (Primary) -Decreased (Secondary) * T4 low * Supplement
49
Hashimoto Thyroiditis (4)
* Autoimmune * Painless enlargement * Symmetric & diffuse * Risk of B-cell non- Hodgkins Lymphomas
50
ETIOLOGICAL AND CLINICAL ASPECTS OF HYPERTHYROIDISM Clinical signs and symptoms (7)
Goiter (small) Exophtalmus (frequent) Heat intolerance Weight loss Malabsorption and diarrhea Tachycardia Irritability and anxiety
51
ETIOLOGICAL AND CLINICAL ASPECTS OF HYPERTHYROIDISM Most common causes (2)
Autoimmune - Graves’ disease and Hashimoto’s thyroiditis
52
ETIOLOGICAL AND CLINICAL ASPECTS OF HYPERTHYROIDISM Laboratory (3)
T4 and Free T4 elevated T3 and Free T3 elevated TSH and TRH suppressed
53
symptoms of hyperthyroidism (5)
weight loss nervousness rapid pulse goiter muscle wasting
54
hyperthyroidism
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
55
Hyperthyroidism Graves Disease (5)
* Tachycardia * Increased appetite * Weight loss * Exophthalmos * Intolerance to heat
56
Hyperthyroidism Graves Disease * Diagnosis (2)
* TSH - Primary-low - Secondary- normal to high * T4 (T3) increased
57
Hyperthyroidism Graves Disease Treatment
* Ablation
58
Hyperthyroidism Graves Disease * Significance (5)
* Thyroid storm * Caused by infection, stress, trauma * Elevated body temp. * Tachycardia * 20-40% mortality
59
Diffuse & Multinodular Goiter (4)
* Thyroid enlargement * Impaired synthesis of thyroid hormone * Maintenance of minimal function (euthyroid) * Diffuse early on, then nodular
60
* Impaired synthesis of thyroid hormone (2)
* Iodine deficiency - Endemic * Hyperplasia of follicles - Pituitary stimulation
61
Sequence Of Events In Endemic Goiter (4)
* Diet deficient in iodine * Decreased output of T3 & T4 by thyroid * Pituitary responds by secreting TSH * Thyroid hyperplasia
62
Thyroid Neoplasms * Adenoma (4)
* Solitary * Males * Younger * Warm/Cold nodules
63
Thyroid Neoplasms * Papillary Carcinoma (5)
* 75-85% * All ages * Radiation * 10 yr = 95% * Worse in elderly
64
Thyroid Neoplasms * Follicular Carcinoma (4)
* 10-20% * Older * Iodine deficiency * Cold nodules
65
Thyroid Neoplasms * Medullary Carcinoma (5)
* 5% * Neuroendocrine * Calcitonin (C cells) * Amyloid * MEN 2 A/B (20%)
66
PARATHYROID GLANDS (4)
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
67
PTH: (5)
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.
68
Hypoparathyroidism (3)
*Surgically induced - Iatrogenic *Congenital absence - DiGeorge Syndrome *Autoimmune - APECED
69
Hypoparathyroidism (3)
Hypocalcemia Chvostek Sign Trosseau sign
70
*Hypocalcemia
*Tetany
71
*Chvostek Sign
*Tapping CN VII - Muscle contraction - Eye, mouth, nose
72
*Trosseau sign
*Occluding circulation of forearm - Carpal spasm
73
Hyperparathyroid Pathology * Primary (3)
* Adenoma (75-80%) - One gland * Hyperplasia (10-15%) - Multiglandular - MEN 1 & 2a,b * Carcinoma (<5%)
74
Hyperparathyroid Pathology * Secondary
* Renal failure - Hyperphosphatemia - Chronic hypocalcemia - Vitamin D deficient
75
PRIMARY HYPERPARATHYROIDISM (4)
Adenoma Hyperplasia Carcinoma Serum calcium levels, especially Ionized calcium levels are high
76
PRIMARY HYPERPARATHYROIDISM Morphologic changes (5)
Skeletal changes - bone resorption - Formation of bone cysts and hemorrhages (osteitis fibroso –cystica) - Brown tumors -Urinary tract stones (nephrolithiasis) - Metastatic calcification
77
Primary Hyperparathyroidism (3)
*Hypercalcemia * Hypophosphatemia * Increased urinary excretion of both calcium and phosphate
78
SECONDARY HYPERPARATHYROIDISM (2)
Calcium is chronically depressed and low serum calcium levels lead to compensatory hyperactivity of the parathyroids Serum phosphate levels are elevated
79
SECONDARY HYPERPARATHYROIDISM Causes (4)
Chronic renal failure Vitamin D deficiency Inadequate dietary calcium Steatorrhea
80
SECONDARY HYPERPARATHYROIDISM Morphology (3)
Hyperplastic parathyroid glands Bone chages (see primary hyperparathyroidism) Metastatic calcification
81
SECONDARY HYPERPARATHYROIDISM Clinical features (5)
Not as severe as in primary hyperparathyroidism Related to symptoms secondary to chronic renal failure Bone abnormalities (renal osteodystrophy) Calciphylaxis Tertiary hyperparathyroidism
82
Hyperparathyroidism (5)
* Osteomalacia & loss of lamina dura * Brown tumor * Nephrolithiasis * Peptic/duodenal ulcers * Mental changes
83
PTH Actions (6)
* 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
Zona Glomerulosa (2)
* Aldosterone * Regulated by angiotensin II
85
Zona Fasiculata (2)
* Glucocorticoids (cortisol) * Regulated by ACTH (biofeedback)
86
Zona Reticularis (2)
* Androgens * No feedback with ACTH
87
Adrenal Cortex Pathology Too Little (3)
* Adrenal insufficiency - Acute - Waterhouse-Friderichsen * Primary Chronic - Addison Disease * Secondary
88
Adrenal Cortex Pathology Too Much (3)
* Hyperaldosterism * Hypercorticolism – Cushing Syndrome * Adrenogenital syndrome
89
Hypoadrenocorticism Addison’s Disease (11)
* 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
* GI disturbances (5)
* Nausea/ Vomiting (N/V) * Anorexia * Diarrhea * Weight Loss * Salt cravings ( K+ ↑, Na+↓,)
91
* Hyper-pigmentation (Bronzing) (2)
* ACTH precursor stimulates melanocytes * Frictional areas
92
* Adrenal Crisis (Acute) (3)
* Abdominal pain * Hypotension * Vascular collapse
93
Hypercortisolism *Primary (6)
* 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
Hypercortisolism *Secondary (4)
* Most common * Exogenous * Rule of 2s * Can become hypocortisol without taper
95
Hypercortisolism (Cushing syndrome) (11)
* Presentation * Central obesity * Peripheral wasting * Buffalo hump * “Moon facies” * Abdominal striae * Hirsutism * Poor wound healing * Diabetes * Hyperglycemia * Osteoporosis * Hypertension
96
Adrenal Neoplasms Cortex * Adenomas (3)
* Cushing * Hyperaldosteronism * “Incidentalomas”
97
Adrenal Neoplasms * Carcinomas (3)
* Rare * Virilizing adenoma * Li-Fraumeni & Beckwith- Wiedemann
98
Adrenal Neoplasms Medulla (3)
* Pheochromocytoma * Neuroblastoma * 10% tumor * 10% Familial (MEN 2A,B) * 10% extra-adrenal * 10% are bilateral * 10% are malignant
99
* MEN 1- AD; Chr 11q (TSG) (3)
* Pancreas (95%): insulinomas, gastrinomas * Parathyroid (40%): hyperplasia * Pituitary (30%): Prolactinomas
100
* MEN 2A- AD; Chr10q (RET proto-onco gene) (1)
* Adrenal Medulla (50%); Med.Thy.Ca.; PT- hyperplasia
101
* MEN 2B (1)
* MEN 2A + marfanoid habitus; mucosal neuromas
102
MEN 2B (5)
* AD * Marfanoid body type * Medullary thyroid carcinoma * Pheochromocytomas * Neuromas
103
* Pheochromocytomas (1)
* Adrenal medulla
104
* Neuromas (4)
* Can be first sign * Soft painless papules * Lips, conjunctiva, tongue, palate, buccal mucosa * Sentinel neuromas
105
Pancreas * Exocrine Pancreas (4)
* Secretes enzymes - Digestion - Inactive proenzymes * Acute pancreatitis * Chronic pancreatitis * Cancer
106
Pancreas * Endocrine Pancreas (3)
* Secretes hormones - Glucose homeostasis - Other metabolic activities * Diabetes mellitus - Beta cells in the islets of Langerhans
107
Acute Pancreatitis (3)
* Injury to acinar cells * Interstitial or edematous pancreatitis - Mild, Reversible * Acute hemorrhagic pancreatitis - Alcoholism, Chronic biliary disease
108
Acute Pancreatitis Etiology * Metabolic (5)
* Alcoholism * Hyperlipoproteineimia * Hypercalcemia * Drugs- Thiazide diuretics * Genetic
109
Acute Pancreatitis Etiology * Mechanical (3)
* Trauma * Gallstones * Iatrogenic injury - Perioperative injury - Endoscopic procedures with dye injections
110
Acute Pancreatitis Etiology * Vascular (3)
* Shock * Atheroembolism * Polyarteritis nodosa
111
Acute Pancreatitis Etiology * Infectious (3)
* Mumps * Cocksackievirus * Mycoplasma pneumoniae
112
Chronic Pancreatitis (5)
* Destruction of pancreatic parenchyma * Intermittent “acute” attacks * Alcoholism * Obstruction of pancreatic duct * Chronic injury to acinar cells
113
* Obstruction of pancreatic duct (4)
* Mechanical blockage * Congenital defects * Cancer * Inspissated mucous
114
Exocrine Pancreatic Neoplasms (3)
* Pancreatic cystic neoplasm * Pancreatic cancer * Acinar cell carcinoma
115
Endocrine Pancreatic Neoplasms * Islet cell tumors (2)
* Insulinoma * Glucagonoma - Mild diabetes - Rash
116
Endocrine Pancreatic Neoplasms * Pancreatic Gastrinoma
* Zollinger-Ellison Syndrome - Hypersecretion of gastric acid - Peptic ulcers - High blood gastrin
117
is diabetes a single disease
no
118
Endocrine Pancreas * Islets of Langerhans * Alpha cells – * Beta cells –
glucagon insulin - diabetes mellitus
119
Diabetes Mellitus (3)
* Hyperglycemia * 21 million people ( 7% of population) * Loss of insulin (anabolic) results in a catabolic state affecting glucose, fat & protein metabolism
120
* Hyperglycemia (3)
* Lack of insulin (Type 1) * Resistance to insulin (Type 2) * Combination
121
Type 1 Diabetes Mellitus Archaic terminology: def:
* Insulin Dependent DM, juvenile-onset DM * Autoimmune destruction of B cells in the Islets of Langerhans (insulitis)
122
Diabetes Mellitus * Type 1 (6)
* Absolute deficiency * Destruction of Beta cells * Only 10% diabetics * Avg. age of onset- 14 yo * Emergencies Slow progression despite abrupt clinical onset
123
* Emergencies * Acute: * Chronic:
hypoglycemia ketoacidosis
124
Type 1 Diabetes Mellitus *Cause- * Autoimmune (2) * Genetic (2) * Environmental? (1)
* Destruction of β-cells * T cell mediated * Auto-antibodies * 30-70% twin concordance * HLA-DR3, DR4 (90-95%) * Infectious
125
Type 1 Diabetes Mellitus *Diagnosis ( DM1 or 2) (4)
* WNL= 70-120 mg/dL * Any of these * ≥ 200 mg/dL + S/S * Fasting ≥ 126 mg/dL * OGTT ≥ 200 mg/dl (2 hrs)
126
Pathogenesis of Type 1 Diabetes Mellitus * Genetic factors * Autoimmunity * Environmental factors *(2)
* Viruses- Coxsackie B * Chemicals
127
Diagnosis of Diabetes Mellitus (2)
* Fasting venous plasma glucose of >140 mg/dl on more than one occasion * Following ingestion of 75 grams of glucose
128
* Following ingestion of 75 grams of glucose (2)
* 2hr venous plasma glucose concentration >200 mg/dl * At least one glucose value during that period is >200 mg/dl
129
Diabetes Mellitus Type 2 * Adult onset (5)
* “Relative” lack of insulin * 80-90% of diabetics * Insulin resistance * Demographics are changing * Ketoacidosis (rare)
130
* Insulin resistance (3)
* Early Normal blood insulin level * Target tissue Resistance * β-cell dysfunction fails to compensate
131
* Ketoacidosis (rare)
* Coma due to hyperosmolarity
132
Type 2 Diabetes Mellitus * Archaic terminology: * Inadequate secretion of --- from the pancreas * Reduced tissue sensitivity to --- * Initially, * Eventually,
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
Diabetes Mellitus Type 2 *Obesity *Genetics (3)
*50-90% of twins *20-40% of 1st degree * Only 5-7% in population
134
Pathogenesis of Type 2 Diabetes Mellitus * Genetic factors (3) * Glucose metabolism * Beta cell function (1)
* Familial history * Obesity * Hypertension * Impaired release of insulin in response to glucose stimulation
135
DM Type 2 Clinical Progression (6)
* Only after 90% destruction of the 106 β-cells * Polyuria * Polydypsia * Polyphagia * Fatigue/wasting * Ketosis (chronic)
136
* Ketosis (chronic) (3)
* Ketone bodies (alternative energy source) * Ketoacidosis & diabetic coma= DM1 * Hyperosmolar non-ketotic coma= DM2
137
Glycosylated Hemoglobin (Hb A1C) (Glycohemoglobin) (2)
* The fraction of glycosylated hemoglobin in circulating red blood cells * Reflects the degree of hyperglycemia during the preceding 6-8 weeks
138
Pathogenesis of the Complications of Diabetes * Macrovascular disease – * Microvascular disease –
large and medium-sized arteries capillary dysfunction in target organs
139
Macrovascular Disease – (3)
* Heart - myocardial infarction * Brain - stroke * Peripheral vascular disease –lower extremity gangrene
140
Microvascular Disease (3)
* Retina –diabetic retinopathy * Kidneys –nephropathy * Peripheral nerves - neuropathy
141
Morphology of Diabetes and Late Complications * Great variability among patients in (4)
* Time of onset * Severity * Organs involved * Tight glycemic control delays onset
142
In most patients, changes are likely to be found in: (5)
* Arteries (macrovascular changes) * Basement membrane of small vessels (microangiopathy) * Kidneys (diabetic nephropathy) * Retina (diabetic retinopathy) * Nerves (diabetic neuropathy)
143
Late complications (3)
* 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
Acanthosis Nigricans definition may be associated with (2)
* 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
Diabetes Mellitus * Oral Complications (5)
* Infections- Candida sp., Mucormycosis, Bacterial * Slow healing * Gingiva- enlargement, erythema * Subjective xerostomia * Parotid gland enlargement
146
Liver * Regenerative (4)
* 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
Liver Functions (6)
Metabolic Synthetic- plasma proteins Storage Degrades/Detoxifies Exocrine Endocrine
148
Metabolic (1)
* Glucose homeostasis
149
* Synthetic- plasma proteins (1)
* Albumin, VLDL, LDL, PT, Fibrinogen
150
* Storage (4)
* Glycogen * Triglycerides * Iron, Copper * Vitamins- A, D, K
151
Degrades/Detoxifies * Phase 1 --- (2) * Phase 2 --- (1)
oxidation * -OH, -COOH * Cytochrome p450
152
Degrades/Detoxifies * Phase 1 --- (2) * Phase 2 --- (1)
oxidation * -OH, -COOH * Cytochrome p450 conjugation * Glucuronic acid= Soluble
153
Exocrine (1)
* Bile (1L/d)
154
Endocrine (4)
* D3 to 25-hydroxy-cholecalciferol * T4 to T3 (active) * GHRH * Insulin & glucagon degradation
155
Causes of Cirrhosis (7)
* One of top 10 causes of death * ETOH * Infection (HBV, HCV) * Biliary disease * Iron overload (Hemochromatosis) * Autoimmune hepatitis * 10% idiopathic
156
Cirrhosis Characteristics (4)
* Diffuse fibrosis and conversion of normal architecture into abnormal nodules * Bridging fibrosis * Parenchymal nodules - Micro (3mm);Macro - regeneration * Entire liver architecture effaced
157
Complications of Cirrhosis (3)
* LOF * Portal hypertension * HCCa
158
Loss of Function (2)
* Hepatocyte death - Loss of Microvilli * Changes in blood flow - Proteins
159
Complications of Cirrhosis * Portal Hypertension (6)
* 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
Portal Hypertension Clinical Consequences (4)
* Ascites * Formation of portosystemic venous shunts * Congestive splenomegaly * Hepatic encephalopathy
161
Complications of Cirrhosis * Ascities (2)
* Fluid in the peritoneum (500mL) * Serous fluid
162
Complications of Cirrhosis * Pathogenesis (5)
* 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
Signs & Symptoms of Liver Failure (6)
* Jaundice * Hypoalbuminemia * Hyperammonemia - NH3 to urea * Hypoglycemia * Estrogen metabolism - Palmar erythema - Spider angioma - Hypogonadism - Gynecomastia * Coagulopathy
164
Jaundice is not a disease (4)
* 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
Causes of Liver Disease (6)
* Alcohol related * Drug related * Infectious (HCV) * Metabolic * Neoplasms * Autoimmune
166
Alcoholic Liver Disease (3)
* ETOH causes 60% of Chronic Liver Disease * ETOH accounts for 40-50% of deaths due to cirrhosis * 5th leading cause of death
167
Forms of liver disease (3)
* Hepatitic steatosis * Alcoholic hepatitis * Cirrhossis
168
Drug-induced Liver Disease (2)
* Predictable(intrinsic) * Unpredictable(idiosyncratic) - Toxicity + immune reaction
169
Hepatocellular Damage
* 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
Drug-induced Liver Disease * Drug induced chronic hepatitis is indistinguishable from other causes (3)
* Alcoholic liver disease * Viral Hepatitis * Need serology to r/o viral
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HAV (6)
* Self limiting * No carrier state * Life long immunity * Vaccine * Epidemics * Rare fatalities (0.1%)
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HBV (5)
* Prolonged incubation * Chronic carrier state * Increased risk of HCCa * Vaccine- Anti-HBs * 2 Billion alive today will be infected
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HCV (5)
* Similar to HBV, but... * More cirrhosis risk * Used to be transfusion related * IV drug related * Early Tx hopeful for cure
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HDV (3)
* 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
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Hemochromatosis (5)
* 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
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Hereditary hemochromatosis (5)
* AR most common * HFE gene on Chr 6p * Regulation of intestinal absorption is lost * Net gain/year of 0.5-1.0 gm
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Acquired hemochromatosis (2)
* Known source of excess iron * Hemolytic anemia associated with ineffective erythropoiesis
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Pancreatic fibrosis (1)
* DM
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Hemochromatosis types (5)
Hereditary hemochromatosis Acquired hemochromatosis Hepatomegaly/dysfunction/Cirrhosis Pancreatic fibrosis Skin pigmentation
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Wilson
* 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
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Wilson * Diagnosis
* 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
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Reye Syndrome (4)
* 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?
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Neoplasms Benign
* Nodular hyperplasia * Vascular injury * Regenerative nodules * Cavernous Hemangioma * Adenoma * Females, BCPs * Rupture is a risk
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Neoplasms Malignant * Metastasis-
* Most common neoplasm IN the liver * Colon * Lung * Breast
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Neoplasms Hepatocellular carcinoma (2)
* Most common neoplasm OF the liver * Cirrhosis precedes (risk factor)
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Hepatocellular Carcinoma (Hepatoma)
* 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)
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Gallbladder
* Located in the upper right quadrant * Stores bile * 50mL * Releases bile * Fat digestion
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Gallbladder Anatomy
* Lacks muscularis mucosae * Submucosa * Mucosal lining * Fibromuscular layer * Subserosal fat * Peritoneal covering
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Gallbladder Disorders (3)
* Cholelithiasis * Cholecystitis * Tumors
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Cholelithiasis
* Cholesterol stones * Crystalline cholesterol monohydrate * Pigment stones * Bilirubin Calcium salts
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Pathogenesis of Cholesterol Stones (4)
* Supersaturated bile with cholesterol * Gallbladder hypomotility * Accelerated cholesterol nucleation * Crystals trapped by gallbladder mucous hypersecretions
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Pathogenesis of Pigment Stones
* Mixture of abnormal insoluble calcium salts of unconjugated bilirubin and inorganic calcium salts
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Cholecystitis * Acute (3)
* Acute inflammation * Obstruction of the neck or cystic duct * Absence of gallstones
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Cholecystitis * Chronic (3)
* Sequel to repeated bouts of acute cholecystitis * Absence of acute cholecystitis * Gallstones
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Tumors (2)
* Carcinoma of the gallbladder * Carcinoma of the extrahepatic bile ducts

Pathology (23 decks)

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