Histology Diseases Test 4

Front 1

Addison's

Back 1

- Hyposecretion of Adrenal Cortex
- Dec. Mineral & Gluco corticoids
- Hypotension
- Dec. fxn to stress
- High ACTH levels

Front 2

Cushing's

Back 2

- Excess Glucocorticoid secretions
- Buffalo Hump, Ab Fat, Moon face
- bruise easily, striae, poor wound healing, susceptible to diabetes
Causes: xcess ACTH, xcess CRH, xcess cortisol or corticosterone

Front 3

Conn's

Back 3

- Excess Mineralocorticoids
- Hypertension, Polyuria, dec K, Inc Na

Front 4

Androgenital Syndrome

Back 4

- Excess Androgen secretion leading to masculinization in females
- 21 or 11 beta hydroxylase deficiency
- results in low glucocorticouds & high ACTH
- Hirsutism, receding hairline, male escutcheon, big clit
* Body secretes lots of ACTH trying to boost glucocorticoids levels and as a side fx makes lots of androgens

Front 5

Pheochromocytomas

Back 5

- adrenal medullary tumors
- cause hypersecretion of NE & Epi

Front 6

Kallman's Syndrome

Back 6

- LHRH (GnRH) neurons do not migrate from olfactory regions to hypothalamus b/c of agenesis of olfactory bulbs.
- No LHRH to stim AP and gondadotropin secretion is hypogonadotropic
- Testes are not stimulated & person is hypogonadal

Front 7

Eunuchoidism

Back 7

- Delayed or absent puberty
- Minimal leydig cell testosterone secretion before puberty
- tall w/ female configuration

Front 8

Cryptorchidism

Back 8

- nondescended testes in one or both sides

Front 9

Klinefelter's

Back 9

- XXY
- Hypogonadism & Infertility
- Small Testes
- Spermatogenesis doesn't get past primary spermatocytes

Front 10

Endometriosis

Back 10

- Ectopic growth of endometrial tissues
- Causes fibrosis and may prevent ovum from entering the abdomen

Front 11

Sheehan's Syndrome

Back 11

- AP is enlarged during preg. due to increased estrogen causing increased lactotrope number & size, which may put pressure on pituitary stalk.
- Causes Shock w/ vascular collapse if there is hemorrhage postpartum in portal vessels
- Hypopituitarism develops
- Patient will feel weak and health will go down hill
- may have trouble lactating
- Secondary Hypothryoidism
- fatigue, weight gain, hair loss

Front 12

When does luteinization start?

Back 12

one day prior to ovulation

Front 13

Chiari-Frommel Syndrome

Back 13

- Persistance of Lactation (galactorrhea) and amenorrhea in women who do not nurse after delivery
- due to increased prolactin secretion & low FSH & LH
- Similar to women w/ prolactin adenomas (most common type of AP tumor)

Front 14

Gynecomastia

Back 14

Breast development in males
- due to increase in circulating estrogen

Front 15

Precocious Puberty

Back 15

- Early puberty due to loss of GnRH regulating mechanism
- GnRH (LHRH) is secreted unregulated
- can be due to hypothalamic lesions

Front 16

Precocious Pseudopuberty

Back 16

- secondary sex characteristics w/out gametogenesis
- due to exposure to androgens or estrogens

Front 17

Primary & Secondary Amenorrhea

Back 17

Primary
- amenorrhea until puberty

Secondary
- amenorrhea after puberty
- stopping of menstrual cycle
- normal during pregnancy & menopause
- can be induced be anorexia or excess weight loss from exercise

Front 18

Acromegaly

Back 18

- Hands/Feet enlarged
- galactorrhea
- Internal organs enlarge
- headaches
- tunnell vision

- Due to a GH or GHRH secreting tumor causing hypersecretion of IGF-1 from the hepatocytes AFTER puberty

Front 19

Gigantism

Back 19

- Caused by hypersecretion of IGF-1 PRIOR to puberty
- GH or GHRH secreting tumor
- Often have hypopituitarism resulting in low Gonadal hormones and failure to close epiphyseal plates

Front 20

Pituitary Dwarf

Back 20

- Due to Hyposecretion of IGF-1 prior to adulthood, low GH, GHRH, or IGF-1
- Can be fixed before closure of epiphyseal plates by administration of GH

Front 21

Laron Dwarf

Back 21

Insensitivity to GH, caused by a mutation in the receptor

Front 22

Creutzfield-Jakob Disease

Back 22

- Using cadavers as a source of GH can cause this disease
- Prion disease
- Degeneratice neurological disorder

Front 23

Achondroplasia

Back 23

- can cause dwarfism
- genetic lack of receptor for fibroblast growth factor receptor
-

Front 24

Kasper- Hauser Syndrome

Back 24

- Failure to produce GH due to neglect stress
- pyschosocial

Front 25

Embryo - Adrenals

Back 25

Cortex - Mesoderm
Medulla - Neural Crest Cells, Ectoderm

Front 26

Embryo - Thyroid

Back 26

Follicular Cells
- Migrate through the floor of the oral cavity & reach anterior side of trachea
- ENDODERM

C-cells
- migrate to anterior side of trachea
- from NEUROECTODERM (neural crest cells)

Front 27

Iodine Deficiency

Back 27

- Goiter
- Can't make T3 or T4
- Prob high TSH levels
- Big columnar follicular cells
- little colloid

Front 28

Hyperthryoidism

Back 28

- usually assoc. w/ graves (low TSH due to TSH receptor stimulating ab)
- can lead to hypertrophy & hyperplasia of thyroid
- rarely is due to a TSH secreting tumor

Front 29

Graves

Back 29

- Hyperthyroidism
- low TSH levels
- assoc. w/ TSH receptor stimulating antibodies (used to be called LATS)
- exophthalamos
-

Front 30

Cretinism

Back 30

- hypothyroidism in children
- irreverisble
- stunted mental & physical growth due to low T3 & T4 due to def. of Iodine

Front 31

Myxedema

Back 31

- hypothyroidism in adults
- assoc w/ low or high TSH
- Can be caused by Iodine def (high TSH)
- Can be caused by compromised pituitary (low TSH)
- Thickened, dry, flaking skin
- Pale, Yellow Skin
- Most commonly in US caused by antibodies against thyroglobulin, thyroperoxidase, or TSH receptor blocking antibody
- Can be diagnosed on phone

Front 32

Diabetes Insipidus
- Congenital & acquired

Back 32

Congenital
- mutation in PP for ADH

Acquired
- one cause is Sheehan's Syndrome

Front 33

Nephrogenic Diabetes Insipidus

Back 33

- ADH may be normal, but kidneys don't respond well

Causes
- Loss of V2 receptor
- abnormal aquaporin 2 channel

Front 34

Diabetes Insipidus in Pregnancy

Back 34

- Placenta makes VASOPRESSINASE
- increases clearance of ADH causing diabetes insipidus

Front 35

SIADH

Back 35

- increased ADH due to a tumor or a disorder
- dec. plasma osmolality
- inc. urine osmolality, very concentrated urine

Front 36

Vit D. Deficiency

Back 36

Rickets - Kids
Osteomalacia - Adults

* bowlegs & knock knees

Front 37

3 Fxns of PTH on Ca

Back 37

1.) inc. bone resorption of Ca, raising blood Ca levels
2.) inc. Ca resorption in distal tubules of kidney
3.) inc. 1,25 dihydroxycholecalciferol (Vit D) causing Ca resorption in gut

Front 38

Hypoparathyroidism

Back 38

- Hypocalcemia (Trousseau's & Chvostek's sign)
- Leads to muscle spasms & tetany

Front 39

Pseudohypoparathyroidism

Back 39

- Plasma PTH high
- defect in receptors for PTH

Front 40

Primary Adrenal Insufficiency

Back 40

- Lack of ACTH receptors on adrenal gland
- High ACTH
- Addison's (Low Cortisol)

Front 41

Secondary Adrenal Insufficiency

Back 41

- No ACTH secretion
- dec. glucocorticoids

Front 42

Hyperparathyroidism

Back 42

- Hypercalcemia
- Hypophosphatemia
- destruction of bones and formation of kidney stones
- primary cause is a benign adenoma, cancer in the glands is less common

Front 43

3 Major Steps of FA Synth

Back 43

1.) Transport of Mitochondrial Acetyl-CoA to the cytosol
2.) Conversion of Acetyl CoA to Malonyl CoA, the "committed step", which activates acetyl CoA
3.)FA synthesis via FA Synthase

Front 44

Citrate Lyase

Back 44

- transports citrate across the OMM and cleaves it into OAA & Acetyl-CoA

Front 45

Isocitrate dehydrogenase in the fed state

Back 45

- It is inhibited in the fed state
- causing accumulation of citrate for FA synthesis

Front 46

Malic Enzyme

Back 46

Malate --> Pyruvate
- regenerates NADPH for FA synthesis

* PPP also regenerates NADPH which can be used in FA synthesis

Front 47

NADPH for FA synthesis

Back 47

- Malic enzyme
- PPP

Front 48

High Insulin/Glucagon Ratio induces synthesis of these 3 enzymes for FA synthesis

Back 48

1.) Malic Enzyme
2.) Citrate Lyase
3.) G6PD (PPP)

Front 49

Acetyl CoA Carboxylase

Back 49

Acetyl CoA --> Malonyl CoA
- For FA synth
- "Committed Step"
- requires Biotin

Front 50

Regulation of ACC

Back 50

1.)Phosphorylation
- Insulin, activates Phosphotase, which removes P, activating ACC
- Glucagon, activates AMP-dependent Protein Kinase, phosphorylating ACC, inactivating it

2. Allosteric
- Citrate (+)
- Palmitoyl CoA (-)

3. Induction/Repression of synthesis
- high insulin/glucagon induces synthesis of FA Synthase

Front 51

Thioesterase

Back 51

- Cleaves Palmitate from the ACP on FA synthase

Front 52

2 key control NZ of FA Synth & Breakdown

Back 52

- ACC
- CPT-I

Front 53

Desaturation of FA, requires these 4 things

Back 53

1.) NADPH
2.) O2
3.) Cyt b5
4.) Cyt b5 Reductase

Front 54

Desaturation & elongation of Linoleic acid produces....?

Back 54

- eicosapentaenoic acid (arachidonic acid)

- Linoleic & linolenic acid are omega 3 & 6 FA from plant oils
- essential FA
- used to make arachidonic acid

Front 55

2 ways to make G-3-P for synth of TAG

Back 55

1.) DHAP --> G3P
- G3P dehydrogenase
- adipose only uses this way
2.) glycerol --> G3P
- Glycerol kinase

* Liver uses both 1 & 2

Front 56

Phosphatidic acid

Back 56

G3P + 2FACoA --> Phosphatidic Acid

- a common precursor for both TAGs & Phospholipids

Front 57

Difference between Muscle LPL & Adipose LPL

Back 57

Muscle LPL
- low Km (high aff.)
- allows m. to use FA as fuel even when [VLDL] is decreased

Adipose LPL
- High Km (low aff.)
- stores fates when [VLDL] is high (ie. after a meal)

Front 58

In adipose tissues, insulin stimulates

Back 58

1. Secretion of LPL
2. Transport of glucose into cells
3. Glycolysis
4. Conversion of glucose to fatty acids

Front 59

Familial combined hyperlipidemia (FCH)

Back 59

Overproduction of apo-B100 = increased VLDL packaging