Pathoma - Section 3 - Fundamentals Of Pathology

Front 1

What is necrosis?

Back 1

Death of large groups of cells followed by acute inflammation.

Front 2

Necrosis is due to some underlying _________ process, it is never _________.

Back 2

pathologic; physiologic

Front 3

What is the morphologic hallmark of cell death?

Back 3

Loss of the nucleus, which occurs via nuclear condensation (pyknosis), fragmentation (karyorrhexis), and dissolution (karyolysis).

Front 4

The two mechanisms of cell death are ________ and ________.

Back 4

apoptosis; necrosis

Front 5

What are the patterns of necrosis?

Back 5

(1) Coagulative necrosis
(2) Liquefactive necrosis
(3) Gangrenous necrosis
(4) Caseous necrosis
(5) Fat necrosis
(6) Fibrinoid necrosis

Front 6

A 67-yo man has had sharp chest pain not relieved by nitroglycerin for the last three hours. What do you expect to see on a CBC?

Back 6

MI. Necrosis is followed by acute inflammation, which increases the white blood cell count.

Front 7

What is coagulative necrosis?

Back 7

Necrotic tissue that remains firm. The cellular proteins "coagulate", so that the cells remain their shape and the organ structure is preserved (because of denatured enzymes). However, the nucleus has disappeared.

Front 8

Coagulative necrosis is characteristic of ischemic infarction of any organ except _________.

Back 8

brain

Front 9

An area of infarcted tissue is often _____ shaped and ______.

Back 9

wedge; pale

Because, as vessels feed into an organ, they dichotomously branch and distribute blood to an area that looks wedge shaped. The wedge points to the area of occlusion.

Front 10

What is red infarction?

Back 10

It's a type of infarction (other being pale) that occurs if blood re-enters a loosely organized tissue (so it can hold the blood, giving it a red color).

The picture shows a testicle that has undergone red infarction (e.g. testicular torsion).

Front 11

In cryptorchidism, there is an increased risk for the undescended testis to undergo __________.

Back 11

testicular torsion

Front 12

The treatment of testicular torsion is ___________. It can be performed as early as ___________ and should be completed by the age of ______.

Back 12

orchiopexy; 6 months; 2 years

Front 13

The MCC of testicular torsion is ____________ or ___________.

Back 13

violent movement; physical trauma

Front 14

Regarding torsion of the testicle, the majority occur between ________ years and ________ years old.

Back 14

12; 18

Front 15

A 15 year old boy comes in to the ER with a chief complaint of a "really bad pain" in his right testicle. It occurred suddenly. As a competent doctor, how would you confirm the diagnosis?

Back 15

Diagnosis is by ultrasound

Front 16

A 14 year old boy from the rural countryside comes in to your office complaining of a strong pain in his left testicle that has lasted for 10 hours. What should you do?

Back 16

Confirm diagnosis with ultrasound. If torsion, perform surgery, it is imperative if the torsion has not remitted (which 1/3 spontaneously do) within 12 hours.

Front 17

You note that the scrotum does not retract when you stroke the inner thigh of a 16 year old boy with a tongue blade. What is this called?

Back 17

Absent cremasteric reflex, seen in testicular torsion.

Front 18

What is liquefactive necrosis?

Back 18

A type of necrosis where the necrotic tissue becomes liquefied. Enzymatic lysis of cells and proteins results in liquefaction.

Front 19

Liquefactive necrosis is seen in three circumstances. What are they?

Back 19

(1) Brain infarction
(2) Abscess (walled off area of dead tissue)
(3) Pancreatitis
• We activate the enzymes of the pancreas within the pancreas itself.

Front 20

Why do we see liquefactive necrosis in the brain?

Back 20

Microglial cells (the "macrophages of the brain") release enzymes that digest the tissue after it has died.

Front 21

What is gangrenous necrosis? What is it characteristic of?

Back 21

It's not a specific pattern of necrosis... it is coagulative necrosis that resembles mummified tissue. It is characteristic of necrosis of the lower limb and GI tract.

Front 22

What is this?

Back 22

Gangrenous (dry) necrosis. Seen often in diabetics who are often subject to ischemic necrosis of the lower limb.

Front 23

What is this?

Back 23

Wet gangrene. Gangrene with superimposed infection.

Front 24

Another word for Buerger's disease?

Back 24

Thromboangiitis obliterans.

Front 25

What is Buerger's disease?

Back 25

A medium-sized vessel vasculitis with digital thrombosis.

Front 26

What is the classic type of patients seen in Buerger's disease?

Back 26

Men 25-5o years old who smoke cigarettes.

Front 27

A 30 year old man with a smoking habit comes in to your office. He says he has lost sensation in his toes and fingers. What should you suspect?

Back 27

Buerger's. It can damage neurons as well.

Front 28

In contrast to the vascular insufficiency caused by atherosclerosis, in Buerger disease the insufficiency tends to be accompanied by _________, even at ________, related undoubtedly to the _________involvement.

Back 28

severe pain; rest; neural

Front 29

Often seen in Buerger's disease is pain in the ________ of the ________, brought on by exercise.

Back 29

instep; foot

Front 30

Regarding thromboangiitis obliterans, in addition to pain, ulceration and possible gangrene with loss of sensation of digits, _______________ may be seen.

Back 30

Raynaud's phenomenon

Front 31

How is Raynaud's phenomenon similar to thromboangiitis obliterans?

Back 31

It's a medium sized vasculitis involving digital vessels in fingers and toes. May also affect tip of nose and ears in some cases.

Front 32

Treatment of Buerger's disease.

Back 32

Smoking cessation is essential. IV iloprost (prostaglandin analogue) may be given. Aspirin.

Front 33

Raynaud's disease is classically seen in what patient group?

Back 33

Young women

Front 34

What artery would rank third as a preferred site of involvement in atherosclerosis?

Back 34

Popliteal artery.

1. Abdominal aorta
2. Coronary artery
3. Popliteal
4. Internal carotid artery

Front 35

What is caseous necrosis?

Back 35

It's basically liquefactive necrosis with something mixed in (like TB or fungus). Is in reality a combination of coagulative and liquefactive necrosis. Characterized by a soft, friable necrotic tissue with "cottage cheese-like" appearance.

Front 36

How is the caseous material in caseous necrosis formed?

Back 36

Caseous material is formed by the release of lipid from the cell walls of M. tuberculosis and systemic fungi (e.g.. Histoplasma) after immune destruction by macrophages.

Front 37

What is fat necrosis?

Back 37

Necrosis of adipose tissue. It has a chalky-white appearance due to deposition of calcium. When fat dies, FAs are released, they have the ability to bind with calcium (this is saponification).

Front 38

What is this?

Back 38

Fat necrosis with white chalky deposits.

Front 39

Fat necrosis is characteristic of what?

Back 39

(1) Trauma to fat (e.g., breast)
(2) Pancreatitis-mediated damage of peripancreatic fat.

Front 40

A woman comes in with complaints of a breast mass. The skin is retracted. A biopsy is performed and shows giant cells, fat and calcification. What do you suspect?

Back 40

Fat necrosis due to trauma. Skin retraction can be seen in this situation and may mimic cancer.

Front 41

The most common cause of breast pain is ____________.

Back 41

fibrocystic change

Front 42

The mean age of breast cancer is _______.

Back 42

64 years old

Front 43

What other pathology of the breast may contain calcifications in addition to fat necrosis?

Back 43

Ductal carcinoma in situ. Commonly contains microcalcifications. In fact, it cannot be detected by mammogram unless it contains microcalcifications. A third eventually invade.

Front 44

Provide an example of saponification.

Back 44

Dystrophic calcification. A dead or dying tissue becomes a nidus for calcium to deposit.

Front 45

What is the serum calcium and serum phosphate in cases of dystrophic calcification?

Back 45

Both normal

Front 46

Provide examples of dystrophic calcification.

Back 46

The cancer outgrows its blood supply, it dies and calcification occurs.

Front 47

In metastatic calcification, the serum ________ or the serum _________ is high.

Back 47

calcium; phosphate

Front 48

Provide five causes of hypercalcemia.

Back 48

(1) Malignancy-induced.
(2) Primary hyperparathyroidism
(3) Hyperthyroidism
(4) Vitamin D3 excess
(5) Paget's disease

Front 49

What is a cause of hyperphosphatemia?

Back 49

Hypoparathyroidism

Front 50

Provide two examples of metastatic calcification.

Back 50

(1) Massive calcification of renal tubular basement membranes in the collecting tlucls (nephrocalcinosis). This can produce nephrogenic diabetes insipidus and renal failure.
(2) Basal ganglia calcification in hypoparathyroidism.

Front 51

What is fibrinoid necrosis? How would it appear on histology?

Back 51

Necrotic damage to blood vessel wall. It would appear pink due to leakage of proteins into the vessel wall.

Front 52

Fibrinoid necrosis is characteristic of what?

Back 52

(1) Malignant HTN
(2) Vasculitis

Front 53

Malignant HTN is defined as a BP of ___________.

Back 53

(equal to or more than) 210/120 mm Hg

Front 54

A pregnant woman in her third trimester presents with HTN of 150/90 and a proteinuria in the nephrotic range. In what vessels would you expect to see fibrinoid necrosis?

Back 54

Placental vessels

Front 55

What is apoptosis?

Back 55

Energy-dependent, genetically programmed cell death. It involves single cells or small groups of cells.

Front 56

Provide three examples of apoptosis.

Back 56

(1) Endometrial cell breakdown after withdrawal of estrogen and progeslerone in the menstrual cycle (hormone-dependent atrophy). Decreased hormonal stimulation inactivates Bcl2.

(2) Loss of miillerian structures in a male fetus due to Sertoli cell synthesis of mullerian inhibitory factor

(3) Removal of virally infected cells by CD8+'s

Front 57

What is the morphology of apoptotic cells?

Back 57

(1) The cell shrinks, and the cytoplasm becomes concentrated within the cell and becomes pink.
(2) Nucleus condenses and fragments.
(3) Apoptotic body will fall from the cell and removed by macrophages.

Front 58

In apoptosis we see ________ (inflammation/no inflammation).

Back 58

no inflammation

Front 59

Apoptosis is mediated by ___________.

Back 59

caspases

Front 60

Corticosteroid destruction of B- and T-cells occur via _______.

Back 60

apoptosis

Front 61

Caspases activate ____________ and _____________.

Back 61

proteases (degrades cytoskeleton, cell shrink) and endonucleases (break down DNA, nucleus shrinks)

Front 62

What pathways activate caspases?

Back 62

(1) Intrinsic mitochondrial pathway. Cellular injury, DNA dmg. Cytochrome c mediates this pathway.
(2) Extrinsic receptor-ligand pathway. FAS ligand bind FAS death receptor. TNF can bind TNF receptor as well.
(3) Cytotoxic CD8+ pathway. Perforins and granzymes (activates caspases).

Front 63

Bcl2 __________ (stabilizes/destabilizes) the mitochondrial membrane.

Back 63

stabilizes

Front 64

FAS death receptor is also known as?

Back 64

CD95

Front 65

The BCL2 gene family is located on chromosome _____.

Back 65

18

Front 66

BCL2 gene family manufactures products that ___________.

Back 66

inhibit apoptosis

Front 67

TP53 suppressor gene __________ the cell cycle in the ____ phase to repair DNA damage.

Back 67

arrests; G1

Front 68

BAX gene products _______________ (activate/inactivate) the BCL2 antiapoptosis gene.

Back 68

inactivate

Front 69

Mammalian cells have developed protection to hypoxia. The best defined is ___________ which enhances what?

Back 69

hypoxia-inducible factor-1; new blood vessel formation, enhanced anaerobic glycolysis