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Step 1 Prep > Pathology 2 > Flashcards

Pathology 2 Flashcards

1
Q

Functional unit of ovary

A

Follicle

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2
Q

3 types of cells in the ovary

A

Oocyte, Granulosa, Theca

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3
Q

Which hormone stimulates the theca cells?

A

LH; androgen

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4
Q

Which hormone stimulates the granulosa cells?

A

FSH; converts androgen to estradiol

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5
Q

The 2 phases of the endometrial cycle

A
  1. Proliferative

2. Secretory

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6
Q

The corpus luteum primarily secretes

A

Progesterone

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7
Q

Bleeding into the corpus luteum

A

Hemorrhagic luteal cyst

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8
Q

Degeneration of ovarian follicles leads to…

A

Follicular cysts

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9
Q

Multiple follicular cysts in ovary due to hormone imbalance. Which hormone is increased the most?

A

PCOD; LH:FSH >2

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10
Q

In response to LH, theca cells produce

A

Androgen

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11
Q

Describe hirsuitism and obesity seen in PCOD.

A

Hirsuitism, estrone (peripheral conversion of androgen leads to obesity), negative FSH feedback b/c of high estrone and hence the follicle degenerates

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12
Q

Obese woman with infertility, oligomenorrhea, hirsuitism, insulin resistance (DM2), high risk of endometrial ca

A

PCOD

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13
Q

3 major categories of ovarian tumors

A
  1. Germ cell (oocyte)
  2. Sex cord stromal (G,T)
  3. Surface epithelial
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14
Q

Most common type of ovarian tumor

A

Surface epithelial

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15
Q

Surface epithelial tumors of the ovary are typically derived from…

A

Coelomic epithelium that lines the ovary

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16
Q

Single cystic ovarian mass with simple, flat lining arising in a pre-menopausal woman

A

Benign cyst adenoma

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17
Q

What is the name for tumors in between benign and malignant ovarian tumors?

A

Borderline

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18
Q

BRCA1 mutation carriers most classically p/w what subtype of ovarian carcinoma?

A

Serous cyst AC (ovary & fallopian tube)

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19
Q

Malignant ovarian ca assoc w/ endometriosis. Any other cancer to look for??

A

Endometrioid tumor (of ovary & endometrium!)

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20
Q

Malignant ovarian ca that contains urothelium.

A

Brenner tumor

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21
Q

T/F Surface epithelial tumors generally present late.

A

True

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22
Q

Useful serum marker for ovarian ca treatment/recurrence

A

CA-125

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23
Q

Germ cell tumors of the ovary typically present in women of what age?

A

Reproductive age

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24
Q

5 different types of ovarian germ cell tumors

A
  1. Teratoma (fetal)
  2. Embryonal
  3. Yolk sac
  4. Germ cell (dysgerminoma)
  5. Placental (choriocarcinoma)
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25
Q

Cystic ovarian tumor composed of fetal tissue derived from 2-3 embryologic layers

A

Cystic teratoma [B/L in 10% of patients]

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26
Q

Most common type of immature tissue in an immature teratoma

A

Neuroectoderm

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27
Q

The most common type of somatic malignancy that arises from a malignant teratoma

A

Squamous cell carcinoma of the skin

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28
Q

Cystic teratoma composed primarily of thyroid tissue

A

Struma ovarii

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29
Q

Ovarin tumor: large cells with clear cytoplasm and central nuclei; testicular counterpart is called __________. What is the serum tumor marker?

A

Dysgerminoma; Seminoma

Serum tumor marker LDH

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30
Q

Malignant tumor that mimics the yolk sac; most common germ cell tumor in children. Serum AFP is elevated. What tumor and what is seen on histology?

A

Endodermal sinus tumor

* Schiller-Duval bodies on histology (glomerulus-like structure)

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31
Q

Malignant-like proliferation of placenta-like tissue. Composed of trophoblasts and synctiotrophoblasts without villi.

A

Choriocarcinoma: small, hemorrhagic tumor with early hematogenous spread. High b-HCG; poor response to CTX

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32
Q

Response to CTX: gestational chorioca vs. germ cell chorioca

A

Gestational with very + response

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33
Q

Ovarian germ cell tumor with large, primitive cells; aggressive with early mets

A

Embryonal ca

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34
Q

Sex-cord stromal neoplasm of ovary that often produces estrogen [p/w estrogen excess]

A

Granulosa-theca cell tumor

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35
Q

Sex-cord stromal tumor of ovary that can produce androgen: hirsutism or virilization. What is the characteristic histology?

A

Sertoli-Leydig cell tumor: Reinke crystals [pink cells with crystals]

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36
Q

Sex-cord stromal tumor of ovary with fibroblasts. What is the KEY association?

A
  • Fibroma.

- - Pleural effusion and ascites: Meigs syndrome

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37
Q

Kruckenberg tumor

A

From the stomach (diffuse – signet ring), breast (lobular), colon ca

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38
Q

Mucinous tumor of ovary vs. Kruckenberg

A

Mucinous: unilateral
Kruckenberg: B/L

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39
Q

Pseudomyxoma peritonei tumor is primarliy from

A

Appendix with ovarian mets

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40
Q

Implantation of fertilized ovum at site other than uterine wall; key risk factor

A

Scarring; endometriosis

* Common site: mpulla lumen

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41
Q

Spontaneous abortion presents at what week or before? Classic causes include…

A

20 weeks

* Chromosomal anomalies, hypercoaguable states (SLE), congenital infection, teratogens

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42
Q

Teratogens can lead to:
Until week 2:
Weeks 3-8:
After week 8:

A

Until week 2: spontaneous abortion
Weeks 3-8: malformation
After week 8: hypoplasia

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43
Q

Implantation of placenta in lower uterine segment (overlies cervical os)

A

Placenta previa

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44
Q

Separation of placenta from decidua prior to deliver; p/w 3rd trimester bleeding and fetal insufficiency

A

Placental abrutption

* Still birth

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45
Q

Placenta previa vs. abruption vs. accreta

A

Previa: Internal os
Abruption: Separation
Accreta: Myometrium

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46
Q

Improper implantation of placenta into the myometrium with little or no intervening decidua. p/w difficult delivery of the placenta and post-partum bleeding. Requires hysterectomy

A

Placenta accreta

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47
Q

What is the decidua?

A

Endometrium under the influence of progesterone

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48
Q

Pregnancy induced HTN, proteinuria and edema. Underlying pathophysiology

A

Pre-eclampsia; 2/2 abnormality of MF vascular interface in placenta [GEPH]

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49
Q

Pregnancy induced HTN, proteinuria and edema & seizures.

A

Eclampsia

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50
Q

What is the classic histologic finding in a pregnant woman with pregnancy induced HTN, proteinuria and edema.

A

Fibrinoid necrosis of placental vessels

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51
Q

Pregnancy induced thrombotic microangiopathy associated with pre-eclampsia

A

HELLP

Hemolysis, elevated liver enzymes, low platelets

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52
Q

Risk factors for SIDS (1 month-1 year)

A

Stomach, smoking in households, prematurity

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53
Q

Abnormal conception characterized by swollen and edematous villi with proliferation of trophoblasts

A

Hydatidiform mole; uterus expands faster than normal / b-HCG higher than expected

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54
Q

Passing of grape-like masses through vaginal canal in 2nd trimester

A

Hydatidiform mole

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55
Q

Snow-storm appearance on U/S with absent fetal heart sounds

A

Hydatidiform mole

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56
Q

Partial vs. Complete mole

  • Genetics
  • Fetal tissue
  • Villous edema
  • Trophoblastic proliferation
  • Risk for chorica
A

Complete

  • Genetics: all from dad 46
  • Fetal tissue: absent
  • Villous edema: all!
  • Trophoblastic proliferation: complete!!
  • Risk for chorica: high risk!
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57
Q

What cells make beta-HCG?

A

Synciotrophoblasts

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58
Q

What is monitored to ensure adequate hydatidiform mole removal?

A

Beta-HCG

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59
Q

The key complication to screen for following a choriocarcinoma

A

Gestational choriocarcinoma

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60
Q

Do you see villi in a choriocarcinoma?

A

No

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61
Q

Secondary amenorrhea 2/2 loss of basalis of endometrium and subsequent scarring. What is the syndrome and what is the cause?

A

Syndrome: Asherman
Cause: Overaggressive D & C

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62
Q

Lack of ovulation; results in estrogen-driven proliferative phase w/o progesterone-driven secretory phase; common cause of dysfunctional uterine bleeding during menarche and menopause

A

Anovulatory cycle

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63
Q

Common cause of acute endometritis

A

Retain products of conception

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64
Q

Characteristic cell seen in chronic endometritis

A

Plasma cell

Arises 2/2 retained products, PID, IUD, TB

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65
Q

Hyperplastic protrusion of endometrium that p/w abnormal uterine bleeding. What is the high yield cause?

A

Endometrial polyp 2/2 AE of Tamoxifen

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66
Q

Endometrial glands AND stroma outside the endometrial lining p/w dysmenorrhea and pelvic pain

A

Endometriosis

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67
Q

3 theories of endometriosis

A
  1. Retrograde menstruation
  2. Metaplastic (Mullerian duct derivatives)
  3. Lymphatic dissemination (can see in lung!)
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68
Q 
Common sites of involvement of endometriosis:
**Ovary
Uterine ligaments
Pouch of Douglas
Bladder wall
Bowel serosa (gunpowder lesions)
Fallopian tube mucosa
A 
Ovary: chocolate cyst
Uterine ligaments: pelvic pain
Pouch of Douglas: defacation
Bladder wall: urination
Bowel serosa: Abdominal pain/adhesions
Fallopian tube mucosa: scarring
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69
Q

Endometriosis in the myometrium is called

A

Adenomyosis

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70
Q

Does endometriosis increase risk of ovarian cancer?

A

Yes

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71
Q

Hyperplasia of endometrial glands relative to stroma is driven by:

A

Endometrial hyperplasia: ESTROGEN

- P/W post-menopausal uterine bleeding

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72
Q

Most important predictor for progression to carcinoma in endometrial hyperplasia

A

Cellular atypia

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73
Q

2 pathways of endometrial carcinoma. What is the classical histology of each?

A
  1. Hyperplasia: fat, young
    * Endometrioid sub-type
  2. Sproadic: skinny, old
    * Atrophic [serous/papillary histology – psammoma bodies]
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74
Q

The sporadic pathway of endometrial cancer is driven by what mutation?

A

p53 mutations

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75
Q

Can sporadic endometrial cancer lead to psammoma body formation?

A

Yes

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76
Q

Psammoma body formation (4) cancers

A
  1. Papillary ca thyroid
  2. Meningioma
  3. Papillary serous ca ovary
  4. Mesothelioma
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77
Q

Benign proliferation of smooth muscle arising from myometrium in pre-menopausal women who p/w multiple, well-defined white whorly masses

A

Leiomyoma

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78
Q

Most common symptom of leiomyoma

A

Asymptomatic (can cause abnormal UB, infertility, pelvic mass)

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79
Q

Malignant proliferation of smooth muscle arising from myometrium; arises de novo in a post-menopausal woman; single lesion with nex/hemorrhage

A

Leiomyosarcoma

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80
Q

The neck of the uterus is called

A

The cervix

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81
Q

Endocervix, Exocervix epithelium; transformation zone

A

Endo: columnar
Exo: squamous

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82
Q

E6, E7 of high risk HPV

A

p53, Rb

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83
Q

T/F Phosphorylated Rb releases E2F

A

True

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84
Q

T/F Hyperphosphorylated Rb leads to unregulated cell growth

A

True

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85
Q

Secondary risk factors for cervical cancer (besides HPV)

A

Smoking, immunodeficiency

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86
Q

2 important cancers that can be caused by smoking [non-classically]

A
  1. Cervical

2. Pancreatic

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87
Q

Can HPV cause cervical AC?

A

Yes [not picked up by pap smear]

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88
Q

T/F Cervical ca can often p/w hydronephrosis

A

T

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89
Q

One of the most common causes of death in cervical ca

A

Renal failure 2/2 hydronephrosis

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90
Q

Abnormal pap smear is followed by…

A

Colposcopy and bx

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91
Q

2 major limitations of pap smear

A
  1. Not at transformation zone [false negative]

2. Does not detect AC

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92
Q

Quadrivalent HPV immunization covers against

A

HPV 6, 11, 16, 18

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93
Q

Focal persistence of columnar epithelium in the upper vagina is called ____________. What is the major risk factor?

A
  1. Vaginal adenosis

2. DES exposure in utero

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94
Q

Vaginal derivatives
Upper 2/3
Lower 1/3

A

Upper 2/3: Mullerian duct [cervix, uterus]

Lower 1/3: UG sinus

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95
Q

During development, the Mullerian duct’s epithelium (name it) is replaced by (name it)

A

Originally: columnar

Replaced by: st. squamous

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96
Q

Rare complication of DES-associated vaginal adenosis

A

Clear cell adenocarcinoma

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97
Q

Key complications DES daughters & mom’s

A

Daughters:

  1. Clear cell AC
  2. Pregnancy/gestational [smooth muscle problems]

Mom’s: BRCA

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98
Q

Malignant mesenchymal proliferation of immature skeletal muscle p/w bleeding & grape-like mass protruding from vagina or penis of child < 5 yo

A

Embryonal rhabdomyosarcoma (Sarcoma boytrides)

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99
Q

Embryonal rhabdomyosarcoma histology and IHC

A
  • Rhabdomyoblast with cytoplasmic cross-striations

- Positive IHC for desmin and myogenin

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100
Q

Cancer from lower 1/3 of vagina goes to what LN

A

Inguinal nodes [UG sinus]

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101
Q

Cancer from upper 2/3 of vagina goes to what LN

A

Iliac nodes [Mullerian duct]

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102
Q

Cystic dilation of Bartholin gland usually unilateral and in the lower portion of the vaginal vestibule

A

Bartholin cyst 2/2 inflammation in a woman of repro age

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103
Q

Warty neoplasm 2/2 HPV 6, 11 characterized by koilocytic change

A

Condyloma accuminatum

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104
Q

How is HPV classfied into high and low risk?

A

DNA sequencing [6, 11 vs. 16,18, 31, 33]

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105
Q

Thinning of epidermis and fibrosis of dermis; leukoplakia with parchmant-like vulvar skin in post-menopausal .

A

Lichen sclerosis

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106
Q

Lichen sclerosis: any increased risk of squamous cell carcinoma?

A

Yes: slightly increased risk

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107
Q

Hyperplasia of vulvar squamous epithelium; leukoplakia with thick, leathery vulvar skin associated with chronic irritation/scratching

A

Lichen simplex chronicus

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108
Q

Lichen sclerosis vs. Lichen simplex chronicus

A

Sclerosis: thinning-parchmant, inc. risk
Simplex: thickening-leather, no inc. risk

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109
Q

Does vulvar carcnioma p/w leukoplakia?

A

Yes

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110
Q

What are the 2 pathways of vulvar carcinoma? What are the risk factors for each?

A
  1. HPV
  2. Non-HPV
    * Long-standing lichen sclerosis
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111
Q

Malignant epithelial cell in epidermis of the vulva that p/w erythematous, pruritic, ulcerated skin that represents carcinoma in situ, but not necessarily underlying cancer

A

Extra-mammary Paget Disease

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112
Q

What is the DDX of extra-mammary Paget disease? What IHC stains can help you tell the difference?

A

Melanoma: PAS-, keratin-, S100+
Carcinoma: PAS+, keratin+, S100-

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113
Q

Goal of primary hemostasis & secondary hemostasis

A

Platelet plug; stabilize the plug

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114
Q

The step just prior to primary hemostasis is mediated by

A

Transient vasoconstriction [neural stimulation & endothelin]

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115
Q

VWF binds to

A

Sub-endothelial collagen & gp1b (adhesion)

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116
Q

VWF comes from

A

Platelet itself & endothelilal cells [Weibel Paliade body]

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117
Q

Weibel Paliade body contains

A
  1. P-selectin

2. VWF

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118
Q

2 mediators released by de-granulated platelets

A
  1. ADP (dense core granules) that promotes gp2b/3a expression
  2. TXA2 (COX)
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119
Q

ADP induces platelets to express

A

Gp2B/3a for platelet aggregation

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120
Q

Platelets link to one another through what molecule?

A

Fibrinogen

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121
Q

Four steps of primary hemostasis

A
  1. Vasoconstriction
  2. Adhesion
  3. Degranulation
  4. Aggregation
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122
Q

A pt w a disorder of primary hemostasis p/w

A

Mucosal (nose, cough, GI, hematura, menstrual) and skin bleeding [petechiae, purpura, eccymoses > 1 cm]; easy bruising

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123
Q

Severe thrombocytopenia can result in this worrisome complication

A

Intracranial bleeding

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124
Q

Do patients with qualitative disorders of platelets get petechiae?

A

No; only quantitative

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125
Q

What are the useful laboratory studies in a patient with bleeding?

A

Platelet count, bleeding time, blood smear, bone marrow bx

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126
Q

Autoimmune production of IgG against platelet antigens [most common cause of thrombocytopenia in children and adults]

A

ITP [Ab-bound platelets are consumed by splenic macrophages resulting in thrombocytopenia]

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127
Q

ITP in childrens vs. adults

A

Children: acute 2/2 viral infection/immunization and self-limiting

Adults: women of child-bearing ages; primary or secondary [SLE]; may cause tbopenia in offspring (IgG)

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128
Q

One of the most important secondary causes of ITP in adults

A

SLE

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129
Q

Lab findings in ITP

A

Low platelets; normal PT/PTT; increased megakaryocytes on BM bx

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130
Q

3 treatment of ITP (3)

A
  • CS: initial
  • IVIG (splenic macrophages start to eat the IVIG to distract them)
  • Splenectomy: eliminate source of Ab and site of destruction
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131
Q

Pathologic formation of platelet microthrombi in small vessels

A

Microangiopathic hemolytic anemia (Schistocytes); platelets are consumed

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132
Q

Any difference between a schistocyte and a helmet cell?

A

No

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133
Q

2 disorders (really one) in which microangiopathic hemolytic anemia is seen

A

TTP & HUS

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134
Q

Why are platelet thrombi formed in TTP?

A

Decrease in ADAMSTS13 enzyme: inability to de-polymerize & degrade VWF

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135
Q

Decreased ADAMSTS13 is usually due to

A
  1. Acquired Auto-Ab

2. Genetics

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136
Q

HUS is due to

A

Endothelial damage by drugs or infection

  • E. coli 0157:H7 [verotoxin] in kidney and brain [exposure to undercooked beef w/ mucusy diarrhea]; also damages ADAMSTS13
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137
Q

Skin and mucosal bleeding, microangiopathic hemolytic anemia, fever, renal insufficiency, and CNS abnormalities

A

TTP/HUS
TTP: neurological
HUS: renal

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138
Q

Lab finding differences between ITP & TTP/HUS

A

Same; TBOpenia, normal coag, anemia with schistocytes, megakaryocytes on BM bx

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139
Q

Treatment of TTP

A

Plasmapheresis and CS

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140
Q

gp1b deficiency & impaired platelet adhesion

A

Bernard-Soulier

* Mild thrombocytopenia with enlarged platelets

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141
Q

Genetic defect of gp2b/3a [platelet aggregation]

A

Thrombasthenia of Glanzmann & Nagelli

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142
Q

Genetic defects of platelet adhesion and aggregation

A

Adhesion: Bernard Soulier
Aggregation: Thrombasthenia of Glanzman Nagelli

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143
Q

ASA irreversibly inactivates

A

COX; lack of TXA2 impairs platelet aggregation

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144
Q

T/F Uremia disrupts platelet function

A

True: adhesion & aggregation

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145
Q

Activation of coagulation factors requires:

A
  1. Exposure to activating substance
  2. Phospholipid surface [platelet surface]
  3. Calcium
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146
Q

Clinical features of 2ndary hemostasis disorders

A

Deep bleeding into muscles and joints; re-bleeding 2/2 surgical procedures

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147
Q

PT vs. PTT

A

PT: extrinsic
PTT: intrinsic

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148
Q

Name the factors in both the intrinsic and extrinsic coagulation cascades

A

12, 11, 9, 8 vs. 7 [10, 5, 2, 1]

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149
Q

What activates factor 12?

A

Sub-endothelial collagen [SEC]

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150
Q

What activates factor 7?

A

Tissue thromboplastin

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151
Q

Heparin monitored with

A

PTT

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152
Q

Warfarin monitored with

A

PT

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153
Q

Genetic XLR of Factor 8

T/F Can arise from a new mutation without any family hx

A

Hemophilia A

* True

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154
Q

Most common coagulation factor inhibitor

A

Anti-Factor 8

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155
Q

Mixing study to differentiate between Hemophilia A & Anti-Factor 8 Ab

A

Mix with normal: Hemophilia results in corrected PTT

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156
Q

Most common inherited coagulation disorder

A

VWF deficiency (AD)

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157
Q

Inheritance of most common inherited coagulation disorder

A

AD: VWF deficiency

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158
Q

Abnormal ristocetin test

A

VWF deficiency

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159
Q

Treatment of VWF deficiency

A

Desmopressin; increases VWF release from WP bodies of endothelial cells

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160
Q

Vitamin K gamma-carboxylates which coagulation factors?

A

2, 7, 9, 10, Factors C + S

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161
Q

Vitamin K deficiency occurs in which patient populations?

A
  1. Newborns (lack of GI colonization)
  2. LTM ABX therapy
  3. Malabsorption
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162
Q

In what organ is epoxide reductase present?

A

Liver

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163
Q

Effect of liver failure on coagulation is followed using: PT or PTT

A

PT

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164
Q

Platelet destruction that arises 2/2 heparin therapy is called:

A

Heparin-induced thrombocytopenia: fragments of destroyed platelets may activate remaining platelets leading to thrombosis

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165
Q

Heparin complexes with… on the surface of platelets (Think HIT)

A

Platelet factor 4

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166
Q

Pathological activation of coagulation cascade: thrombosis and thrombocytopenia

A

DIC

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167
Q

DIC is 2/2

A

Obstetric complication, sepsis, AC [mucin], APML, rattlesnake bite

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168
Q

Which type of leukemia can lead to DIC?

A

APML

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169
Q

Decreased platelets, increased PT, PTT, decreased fibrinogen, microangiopathic hemolytic anemia, elevated fibrin split products

A

DIC

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170
Q

Product of lysed cross-linked fibrin

A

D-dimer (fibrin split product)

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171
Q

Two examples of excessive fibrinolysis.

A
  1. Radical prostatectomy (release of urokinase that activates plasmin)
  2. Cirrhosis of liver (reduced production of alpha-2-antiplasmin)
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172
Q

Alpha-2-antiplasmin

A

Inactivates plasmin (think cirrhosis)

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173
Q

DIC vs. disorder of fibrinolysis

A

Fibrinolysis: normal platelet count; increased fibrinogen split products; no elevation of d-dimers!

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174
Q

Symptoms very similar to DIC without elevated d-dimers

A

Disorder of fibrinolysis

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175
Q

Treatment of disorder of fibrinolysis

A

Aminocaproic acid

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176
Q

Most common location of a thrombus

A

DVT below the knee

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177
Q

Lines of Zahn & attachment to a vessel wall [what do these help distinguish]

A

Both features help distinguish a thrombus from a post-mortem clot

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178
Q

Lines of Zahn

A

RBC, fibrin, RBC, fibrin

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179
Q

Three major risk factors for thrombosis [Virchow’s triad]

A
  1. Endothelial damage
  2. Stasis: stasis or turbulence of blood flow (non-laminar)
  3. Hypercoagulable state
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180
Q

3 examples of stasis (Virchow’s triad)

A
  1. Immobilizaton
  2. Cardiac wall dysfunction
  3. Aneurysm
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181
Q

PGI2 and its vasoprotective effect

A

PGI2 blocks platelet aggregation

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182
Q

Anti-thrombin 3 inactivates

A

Factor 10 and thrombin

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183
Q

Thrombomodulin

A

Redirects the function of thrombin to activates protein

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184
Q

3 major causes of endothelial damage (Virchow’s triad)

A
  1. Atherosclerosis
  2. Vasculitis
  3. High levels of homocysteine
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185
Q

High levels of homocysteine can increase risk for thrombosis. Give several examples

A
  1. B12/Folate deficiency

2. Cystathionine beta synthase deficiency; Homocystinuria

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186
Q

Cystathionine beta synthase deficiency

A

Results in homocystinuria; characterized by vessel thrombosis, mental retardation, lens dislocation and long, slender fingers

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187
Q

6 major causes of hypercoagulable states (Virchow’s triad)

A
  1. Lack of protein C/S [Factors 5 & 8]
  2. Factor 5 Leiden
  3. Prothrombin 20210A
  4. AT3 deficiency
  5. Lupus anti-coagulant
  6. OCP
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188
Q

Increased risk for warfarin skin necrosis is seen in patients with

A

Protein C/S deficiency [increased thrombus formation because of uninhibited 2, 7, 9, 10]

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189
Q

The coagulation factors with the very shortest half-life

A

Proteins C + S [and hence an increased risk for the activation of factors 2, 7, 9, 10]

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190
Q

Mutated form of this factor that lacks the cleavage site for deactivation by proteins C & S

A

Factor 5 Leiden: most common cause of inherited hypercoagulable state

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191
Q

Inherited point mutation in prothrombin that results in increased gene expression and promotes thrombus formation

A

Prothrombin 20210A

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192
Q

In patients with an AT3 deficiency, what happens to the PTT when you dose them with heparin

A

PTT does not rise

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193
Q

An intravascular mass that travels and occludes downstream blood vessels

A

Embolism

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194
Q

Most common source of an embolus.

A

Thrombus

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195
Q

The histologic hallmark of an atherosclerotic embolus

A

Cholesterol cleft in the embolus

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196
Q

What type of embolus is associated w/ long bone fractures? What are the presenting features?

A

Fat embolus

* Dyspnea & petechiae on the skin overlying the chest

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197
Q

Decompression sickness can lead to…

A

Gas embolus: Nitrogen precipitates as you ascend; p/w joint and muscle pain [Benz] and respiratory symptoms [Chokes]

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198
Q

The chronic form of gas embolus is called…

A

Caisson disease: characterized by multifocal ischemic necrosis of the bone

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199
Q

T/F Laparacopic surgery can lead to a gas embolus

A

T

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200
Q

Why can an AF embolus lead to DIC?

A

Tissue thromboplastin in the amniotic fluid [squamous cells and keratin debris from fetal skin]

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201
Q

Keratin debris in the blood vessel of the lung of a female

A

AF embolus

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202
Q

Most common source of DVT

A

Femoral, iliac or popliteal vein

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203
Q

T/F Most PE is clinically silent

A

T

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204
Q

What % of PE cause pulmonary infarction?

A

10%

* Pre-existing CP compromise

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205
Q

T/F D-dimer is elevated in PE

A

T

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206
Q

What does gross exam of a PE demonstrate?

A

Hemorrhagic, wedge-shaped infarct

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207
Q

What type of PE leads to sudden death?

A

Saddle embolus

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208
Q

Chronic pulmonary emboli can lead to…

A

Pulmonary HTN

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209
Q

Systemic embolism usually arise in the… ? Where is the most common site of occlusion?

A

Left heart; lower extremities

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210
Q

Hb values for anemia in males vs. females

A

M: < 13.5
F: < 12.5

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211
Q

MCV values in different anemias

A

Microcytic: < 80
Normocytic: 80-100
Macrocytic: > 100

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212
Q

T/F Microcytosis is due to an “extra” division 2/2 decreased production of Hb

A

True: heme or globin

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213
Q

4 major causes of microcytic anemia

A
  1. Fe deficiency & 2. ACD
  2. Sideroblastic anemia
  3. Thalassemia
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214
Q

Lack of ____ is the most common nutritional deficiency in the world

A

Fe

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215
Q

Iron is consumed in heme and non-heme. Which is meat derived?

A

Heme & more readily absorbed

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216
Q

Fe is absorbed in the …

A

Duodenum; enterocyte

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217
Q

Transporter/key regulatory step in Fe absorption biochemistry

A

Ferroportin [no way to get rid of Fe] ** major site of absorption **

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218
Q

________________ transports Fe & delivers it to the liver and bone marrow macrophages for storage

A

Transferrin

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219
Q

Stored IC Fe in liver and macrophages is bound to…

A

Ferritin

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220
Q

Fe-deficiency anemia

* Infants, children, adults, elderly

A

Infants: breast feeding
Children: poor diet
Adults: M- PUD; F- Menorrhagia/Pregnancy
Elderly: Colon polyps/carcinoma; hookwork (developing world)

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221
Q

The 2 hookworms associated with Fe-deficiency anemia

A

Necator, Ancylostoma

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222
Q

Fe2+ or Fe3+: which is more easily absorbed? Why is this clinically relevant?

A

Fe2+ : maintained by the acidity of the stomach [decreased Fe2+ w/ GASTRECTOMY]

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223
Q

Stages of Fe deficiency

A
  1. Storage depleted
  2. Serum depleted
  3. Normocytic anemia
  4. Microcytic, hypochromic anemia
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224
Q

T/F The initial stage of Fe-deficiency anemia is normocytic

A

True

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225
Q

What is RDW?

A

The spectrum of size of RBC’s

  • Low is normal
  • High is abnormal
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226
Q

RDW in Fe-deficiency anemia

A

Increased

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227
Q

Increase/Decrease: Free erythrocyte protoporphyrin in Fe-deficiency anemia

A

Increased

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228
Q

Fe-deficiency anemia with esophageal web & atrophic glossitis. P/W Anemia, dysphagia and beefy-red tongue

A

Plummer-Vinson Syndrome

[redundancy of esophageal mucosa]

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229
Q

Chronic disease results in increased acute phase reactants. Which one of these is associated with ACD?

A

Hepcidin: sequesters Fe in storage sites; limits Fe transfer from macrophages to erythroid precursors; suppresses EPO production

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230
Q

Increase/Decrease: Free erythrocyte protoporphyrin in ACD

A

Increased

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231
Q

Treatment of ACD in cancer

A

EPO

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232
Q

First step in heme synthesis is RLS. What vitamin is a co-factor?

A

Succ CoA –> ALA

* ALAS / B6 *

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233
Q

Second step in heme synthesis.

A

ALA –> Porphobilinogen

* ALAD *

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234
Q

Ferrochelatase is located in what part of the cell?

A

Mitochondria

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235
Q

T/F If protoporphyrin is deficient, Fe remains trapped in mitochondria

A

True

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236
Q

What is the classical cell seen in sideroblastic anemia? Where is the Fe present?

A

Ringed-sideroblast [iron-laden mitochondria form a ring around the nucleus of erythroid precursors]

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237
Q

What special stain marks iron?

A

Prussian blue

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238
Q

Most common congenital defect in sideroblastic anemia?

A

ALAS deficiency

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239
Q

Acquired casues of sideroblastic anemia

A

EOTH, lead poisoning [ALAD, ferrochelatase], vitamin B6 deficiency

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240
Q

T/F Sideroblastic anemia is an Fe-overloaded state

A

True

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241
Q

Carriers of the thalassemia trait are protected against which species of malaria?

A

Plasmodium falciparum

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242
Q

The 3 normal types of Hb seen in humans.

A

HbA: Alpha2, beta2
HbF: Alpha2, gamma2
HbA2: Alpha2, delta2

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243
Q

There are how many copies of the alpha gene in Hb? What chromosome? What is the genetic defect in alpha-thal?

A

4 in Chromosome 16

* Gene deletion

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244
Q

1-4 genes deleted in alpha-thal. What are the clinical features of each.

A

1: asymptomatic
2: mild anemia with inc. RBC
[cis vs. trans] Cis is worse than trans, particulary for offspring in Asians [seen in Asians]
3: severe anemia (HbH)

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245
Q

cis vs. trans 2x alpha-thal

A

Cis is worse: Asians [offspring]

Trans: Africa

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246
Q

What is HbH?

A

Tetramers of beta chains. Seen on 3-gene deletion alpha-thal.

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247
Q

Hb Barts

A

Hydrops fetalis; tetramer of gamma. Lethal in utero.

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248
Q

Whereas alpha thal is 2/2 gene deletions, beta thal is 2/2

A

Mutations of genes: Ch. 11

[beta null vs. beta plus]

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249
Q

Mildest form of beta thalassemia

A

Beta - Beta+ (Mildest form of disease); target cells

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250
Q

The key finding in Hb electrophoresis in beta thalassemia

A

Increased HbA2, HbF

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251
Q

In beta-thal major, when does baby p/w severe anemia?

A

A few months after birth

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252
Q

Alpha tetramers are seen in alpha or beta thal?

A

Beta thal –> ineffective erythropoiesis

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253
Q

Why is there skull and facial bone abnormalities in patients with beta thal, i.e. crew cut X-ray & chipmunk facies?

A

Expansion of hematopoeisis into marrow of skull and facial bones; extramedullary hematopoesis with HSM; risk of aplastic crisis with parvovirus b19

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254
Q

Aplastic crisis vs. aplastic anemia

A

Crisis: Parvovirus B19 – erythroid precursors

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255
Q

Are target cells seen in beta thal?

A

Yes

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256
Q

Why do you see nucleated RBC’s in thal?

A

If there is extramedullary hematopoeisis & HSM, some of the RBC’s escape

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257
Q

Vitamin B12 passes its methyl group onto…

A

Homocystiene –> Methionine

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258
Q

How many lobes are there in hyper-segmented neutrophils?

A

> 5

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259
Q

Folate is obtained from green vegetables and fruits and is absorbed in…

A

Jejunum

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260
Q

B12 is obtained from animal-derived proteins. It is then cleaved from the proteins & complexes it with ____________ from salivary gland? How and then where is it absorbed?

A

R-binder

  • Pancreatic protease cleaves, then binds with IF; absorbed in ileum
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261
Q

Years to develop B12 deficiency or B9?

A

B12 (strict vegan)

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262
Q

1 cause of B12 deficiency

A

Pernicious anemia

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263
Q

Other causes of B12 deficiency aside from pernicious anemia

A

Pancreatic insufficiency (R-binder proteases)

  • Crohn’s or Diphyllobothrium
  • Strict vegan
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264
Q

Sub-acute combined degeneration of spinal cord

A

2/2 methylmalonic acid; B12 deficiency

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265
Q

How do you differentiate between peripheral destruction or underproduction of RBC in normocytic anemia?

A

Retic count

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266
Q

Why are retics blue on peripheral smear?

A

RNA within cytoplasm

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267
Q

T/F Retic count is falsely elevated in normocytic anemia.

A

True (BM has not made any extra RBCs). Needs to be corrected * Mult by HCT/45

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268
Q

Why is 3% the golden percentage when considering normocytic anemia?

A

3% good marrow response (peripheral destruction)

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269
Q

Hemolyis: IV vs. EV

A

IV: within BV
EV: RES/macrophages liver, spleen, LN

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270
Q

In extravascular hemolysis, the following are broken down to:

A

Globin: AA
Heme: Fe, protoporphyrin
Protoporphyrin: UC bilirubin

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271
Q

What binds free Hb in blood?

A

Haptoglobin

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272
Q

Days after a patient presents with hemoglobinura, he can present with what in his urine?

A

Hemosiderinuria

* Hb taken up by PCT, destroyed and forms hemosiderin; PCT slough off

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273
Q

Inherited defect of spectrin, ankyrin, or band: RBC cytoskeletal membrane tethering proteins

A

Hereditary spherocytosis

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274
Q

Increased RDW with HS?

A

Yes

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275
Q

Increased MCHC with HS?

A

Yes

* Hb becomes more []’ed as cells get smaller

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276
Q

What is work hypertrophy of the spleen?

A

As splenic macrophages work to clear RBC’s in conditions, i.e. hereditary spherocytosis

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277
Q

Osmotic fragility test + in what disease?

A

Hereditary spherocytosis

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278
Q

Howell-Jolly bodies on blood smear

A

Post splenectomy [fragment of nuclear material remaining]

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279
Q

Treatment of hereditary spherocytosis

A

Splenectomy

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280
Q

Inheritance and genetic defect of SCA

A

AR mutation in beta-chain of Hv; normal glutamate (hydrophilic) replaced by valine (hydrophobic)

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281
Q

What is the underlying pathophysiology in HbS?

A

HbS polymerizes when deoxygenated; polymerizes aggregate into needle-like structures resulting in sickle cells [not covalent bonding; reversible]

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282
Q

Increased risk of sickling under what conditions…

Any protective medicine?

A

Hypoxemia, Dehydration, Acidosis

* HbF / hydroxyurea

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283
Q

Target cells in SCA?

A

Yes; redundancy of membrane

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284
Q

Massive erythroid hyperplasia in SCA?

A

Yes

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285
Q

Pathology in SCA is 2/2

A
  1. RBC damage

2. Irreversible sickling

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286
Q

Swollen hands and feet in an African American infant (dactylitis)

A

SCA: common presenting sign 2/2 vasoocclusive infarcts of bones

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287
Q

What patients have an increased risk of Salmonella osteomyelitis?

A

SCA

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288
Q

AA pt p/w chest pain, SOB, lung infiltrates often precpitipated by PNA

A

Acute chest syndrome / SCA

* Vaso-occlusion in pulmonary microcirculation

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289
Q

Most common cause of death in SCA adults

A

Acute chest syndrome

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290
Q

Most common cause of death in SCA children

A

Infection with encapsulated organisms

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291
Q

Can SCA p/w acute papillary necrosis?

A

Yes

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292
Q

What is the one area of the body most susceptible to damage in pts w sickle cell trait?

A

Renal medulla: extreme hypoxia, hypertonicity; microinfarctions; microscopic hematuria and decreased ability to concentrate urine

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293
Q

Metabisfulfite screen

A

Causes cells with any degree of HbS to sickle: both disease and trait

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294
Q

AR mutation in beta chain of Hb where glutamate is replaced by lysine. What do you see on peripheral smear?

A

HbC [ly-seeeeee-ine]

* Characteristic HbC crystals

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295
Q

Acquired defect in myeloid stem cell whereby GPI is no longer present in cell membranes. Results in…

A

Paroxysmal nocturnal hemoglobinura [breath shallow overnight, acidosis / activate complement]

DAF [c3 convertase] & MIRL protect RBC’s against complement ** GPI anchoring protein **

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296
Q

Is PNH genetic or acquired?

A

Acquired

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297
Q

Intravascular or Extravascular hemolysis: PNH

A

Intravascular

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298
Q

Sucrose test is used to screen for…

A

PNH: confirmatory test is acidified serum test of flow cytometery to detect lack of CD55 (DAF)

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299
Q

CD55

A

DAF (GPI-linked membrane protein)

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300
Q

Main cause of death in patients with PNH

A

Thrombosis: destroyed platelets release cytoplasmic contents into circulation inducing thrombosis of hepatic, portal or cerebral veins

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301
Q

Complications of PNH

A

Fe-aneima; AML

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302
Q

XLR disorder that reduces RBC t1/2 and renders cells susceptible to oxidative damage

A

G6PD deficiency
[h2o2 –> glutathione –> h2o]
* NADPH *

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303
Q

2 variants of G6PD

A

Mediterranean: marked reduction
African: Mild

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304
Q

Heinz bodies

A

Oxidative stress (infections, drugs, fava beans) results in (Hb precipitates) Heinz bodies in RBC’s that are removed by the spleen and then you get bite cells

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305
Q

G6PD: Intra or Extravascular hemolysis

A

Intravascular

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306
Q

Hemoglobinuria and back pain

A

G6PD deficiency

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307
Q

How do you screen for G6PD deficiency? How do you confirm it?

A

Heinz preparation; confirm w/ enzymatic studies – not during an episode, but afterward b/c during, all the bite cells will have been consumed

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308
Q

IgM vs. IgG AI hemolytic anemia

A

IgM: Cold, intravascular; fixes complement in extremities
* M. pna, Mono

IgG: Warm, extravascular / spherocytes (similar to HS)
* SLE, CLL, drugs (causes auto-Ab, i.e. methyldopa)

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309
Q

To diagnose hemolytic anemia

A

Coombs test

  • Direct: Anti IgG Ab [are the cells already coated with Ih]
  • Indirect: Does pt have Ab in serum?
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310
Q

What drug is associated with AIHA (warm)

A

Methyldopa

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311
Q

Schistocytes are the hallmark of…

A

Microangiopathic hemolytic anemia [TTP/HUS, ITP, prosthetic valve, AS]

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312
Q

Malaria is transmitted by which mosquito?

A

Anopheles

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313
Q

Daily fever vs. QOD fever in malaria

A

Daily: P. f
QOD: P vivax, ovale

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314
Q

Empty fatty marrow; treatment?

A

Aplastic anemia; drug cesation, transfusion, EPI, GM-CSF, IS, BMT

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315
Q

Pathologic process that replaces bone marrow

A

Myelophthisic process

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316
Q

Myeloid stem cell can produce

A

RBC
Myeloblast (BEN-G)
Monocyte
Megakaryo

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317
Q

2 major causes of neutropenia

A
  1. Drug toxicity

2. Severe infection

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318
Q

Major causes of lymphopenia

A

Immunodeficiency (DiGeorge), high cortisol (apoptosis of lymphocytes), AI destruction (SLE), whole body radiation (most sensitive cell)

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319
Q

Most sensitive cell to whole body radiation

A

Lymphocytes

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320
Q

Neutrophilic leukocytosis

A

Bacterial infection, tissue nex, high cortisol

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321
Q

Cortisol and its effect on blood elements

A

High PMN [less adhesion of marginated PMN’s to endothelium], low lymphocyte

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322
Q

L-shift leukocytosis results in neutrophils with a decreased surface concentration of CD__

A

Immature, decreased Fc receptors [CD16]

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323
Q

CD16

A

Marker of mature WBC’s, decreased Fc receptors [CD16]

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324
Q

Monocytosis

A

Chronic inflammation, malignancy

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325
Q

Eosinophilia

A

Allergy, parasite, Hodgkin lymphoma (IL-5)

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326
Q

Basophilia

A

CML

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327
Q

Lymphocytic leukocytosis is seen in which bacterial infection? Think an unvaccinated child.

A

B. pertussis [lymphocytosis promoting factor]

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328
Q

EBV infection results in lymphocytosis with reactive CD8+ T cells

A

Oropharynx, liver, B cells

  • Mono *
    • LAD, splenomegaly (PALS), high white count with atypical lymphocytes
329
Q

Which part of lymph node is hyperplasied in EBV mono?

A

Paracortex

330
Q

Which part of spleen is hyperplasied in EBV mono?

A

White pulp; PALS (periarterial lymphatic sheath)

331
Q

IgM heterophile Ab are positive with _____

A

Mono; Sheep or horse RBC

Can be negative with CMV

332
Q

Definitive test for mononucleosis

A

EBV viral capsid antigen

333
Q

Complications of mononucleosis

A

Splenic rupture, rash with PCN, dormancy of virus in B cells

334
Q

Acute leukemia requires what percentage of blasts in BM?

A

> 20%

335
Q

Hallmark marker for ALL

A

TdT (DNA polymerase marker)

336
Q

Hallmark marker for AML

A

MPO (Auer rod crystallization)

337
Q

Leukemia & Down Syndrome

A

AML: < 5 yo [megakary]
ALL: > 5 yo

338
Q

B-ALL surface markers

A

CD 10, 19, 20

339
Q

Patients with B-ALL have an excellent response to CTX. However, CTX does not cross several barriers and prophylaxis is required in 2 areas.

A
  1. Scrotum

2. CSF

340
Q

t(12,21) vs. t(9,22) ALL

A

t(12,21): good PGX, more commonly seen in kids

t(9,22): poor PGX, more commonly seen in adults

341
Q

T-ALL surface markers

A

CD2 thru CD8; do not express CD10

342
Q

T-ALL p/w

A

Thymic mass in a teenager (Acute lymphoblastic lymphoma)

343
Q

t(15, 17)

A

t(15, 17) = APML

  • RAR receptor disrupted and promyelocytes acumulate; contain numerous Auer rods and hence increased risk for DIC
  • ATRA causes blasts to mature
344
Q

Acute monocytic leukemia p/w

A

Proliferation of monoblasts; lack MPO & blasts characteristically infiltrate the gums

345
Q

Acute megakaryoblastic leukemia

A

Proliferation of megakaryoblasts; lack MPO; association with Down Syndrome before age 5

346
Q

Myelodysplastic syndromes

A

Cytopenias with hypercellular marrow; abnormal maturation with inc blasts (20% blasts)

Alkylating agents; rads

347
Q

Co-expression of CD5, CD20 leukemia

A

CLL: naive B cells; lymphocytes and smudge cells

348
Q

Smudge cells

A

CLL –> LAD –> SLLymphoma

349
Q

CLL complications

A

Hypogammaglobulimenia, AIHA, Transformation to DLBL

350
Q

TRAP + cells

A

Hairy cell leukemia

* Splenomegaly (red pulp), dry tap, no LAD

351
Q

Splenomegaly with expansion of red pulp and negative LAD and dry tap is seen which which leukemia?

A

Hairy cell leukemia

352
Q

Hairy cell leukemia has an excellent response to what therapy?

A

2-CDA (ADA inhibitor)

Adenosine accumulates to toxic levels in neoplastic B cells

353
Q

HTLV-1

A

ATLL; Cd4+ T cells

* Rash, LAD, HSM, lytic bone lesions with hypercalcemia

354
Q

Lytic bone lesions with hypercalcemia & a rash

A

Multiple myeloma w/o rash, but also HTLV-1 with rash

355
Q

Neoplastic proliferation of mature CD4+ T cells

A

Mycosis fungoides: rash, plaque, nodules

356
Q

Pautrier microabscesses

A

Aggregates of neoplastic T-cells in epidermis in mycosis fungoides

357
Q

Sezary syndrome

A

Characteristic lymphocytes with cerebriform nuclei in mycosis fungoides that spreads to the blood

358
Q

Complications of MDS

A

Hyperuricemia, marrow fibrosis, acute leukemia

359
Q

Basophils are characterizsticaly increased in…

A

CML

360
Q

t(9,22)

A

CML; BCR-ABL fusion [oncogene] with increased TK activity; first line treatment is imatinib

361
Q

Phases of CML

A
  1. Chronic: large spleen
  2. Acceleration: enlarging spleen
  3. Blast: 2/3 to AML, 1/3 ALL
    [mutation in a pluripotent stem cell]
362
Q

When CML progresses to acute leukemia, where is the mutation?

A

CD34+ hematopoietic stem cell

363
Q

CML vs. Leukemoid reaction: LAP

A

CML: LAP negative
CML: basophilia
CML: t(9,22)

364
Q

JAK2 kinase mutation drives which myeloproliferative disorders?

A

PV: blurry vision, thrombosis, flushed face, itching after bathing [mast cells]

& Essential thrombocythemia & MF

365
Q

Treatment PV

A

Phlebotomy, hydroxyurea

366
Q

PV vs. Reactive polycythemia

A

PV: EPO decreased
Reactive: EPO increased
OR RCC with ectopic EPO

367
Q

Increased platelets seen in

A

ET, Fe-deficiency anemia

368
Q

T/F ET rarely progresses to marrow fibrosis, acute leukemia, hyperuricemia

A

True: platelets do not have nuclei!

369
Q

Why does MF have marrow fibrosis?

A

[JAK2] Increased megakaryocytes which produce excess PDGF

370
Q

Leukoerythroblastic smear

A

Myelofibrosis [reticulin gates don’t prevent immature blood cells from leaving the spleen with extra-medullay hematopoesis]

371
Q

Teardrop cell

A

Myelofibrosis

372
Q

Malignant proliferation of plasma cells in bone marrow; most common primary malignancy of bone. What IL is characteristically elevated?

A

MM; serum IL-6 is high

373
Q

Why does MM result in bone pain with hypercalcemia?

A

Neoplastic plasma cells activate RANK receptor on osteoclasts

374
Q

M spike on SPEP. Which Ig?

A

IgG, IgA

375
Q

Multiple myeloma most common cause of death

A

Infection

376
Q

Rouleaux formation of blood smear

A

Multiple Myeloma

377
Q

Free light chain circulating in multiple myeloma results in

A

Primary AL amyloidosis

378
Q

Bence-Jones proteinuria

A

Free light chain in urine in multiple myeloma

379
Q

Isloated M spike without MM signs/symptoms

A

MGUS

380
Q

B cell lymphoma with monoclonal IgM

A

Waldenstrom macroglobulinemia; retinal hemorrhage, stroke, bleeding

381
Q

Pentamer Ig

A

IgM

382
Q

Acute complications of Waldenstrom Macroglobulinemia

A

Plasmapheresis

383
Q

What are Langerhans cells?

A

Specialized dendritic cells found predominantly in the skin; derived from bone marrow monocytes and present Ag to naive T cells

384
Q

Neoplastic proliferation of Langerhans cells

A

Langerhans cell histiocytosis: Birbeck (tennis racket) granules on EM

385
Q

What cells are CD1a and S100+ on IHC?

A

Langerhans cell histiocytosis

386
Q

Skin rash, cystic skeletal defects in an infant < 2 y.o. (Langerhan cell histiocytosis)

A

Letterer-Siew (Malignant proliferation of Langerhans cells)

387
Q

General rules for the subtypes of Langerhans cell histiocytosis

A
  1. Person’s name = Malignant
  2. 2 names = child < 2 y.o.
  3. 3 names = child 3 y.o.
    Skin involvement = malignant
388
Q

Subtypes of Langerhan cell histiocytosis

A
  1. Letterer Siew
  2. Eosinophilic granuloma
  3. Hand-Schuller-Christian
389
Q

Benign proliferation of Langerhans cells in the bone; classic p/w pathologic fx in adolescent; no skin involvement

A

Eosinophilic granuloma

390
Q

Malignant proliferation of Langerhans cells p/w scalp rash, lytic skull defects, DI, exopthalmos in a child > 3

A

Hand Schuller Christian disease

391
Q

Painless inflammation

A

Chronic inflammation, metastatic carcinoma, lymphoma

392
Q

LAD involving:

Follicles, paracortex, sinus histiocytes

A

Follicles: RA, early HIV [follicles]
Paracortex: Viral [mono/EBV]
Sinus histiocytes: LN draining tx w ca

393
Q

Cortex, paracortex, medulla of lymph node. Which cells?

A

Cortex: B cells
Paracortex: T cells
Medulla: sinus histiocytes

394
Q

T/F Lymphoma forms a mass in lymph or extra-nodal tissues

A

True

395
Q

Name the normal zones of the cortex of a lymph node

A

In the corex: Follicle, Mantle, Margin

396
Q

Name the small, medium and large cell lymphomas

A

Small: Follicular, Mantle, Marginal, SLL

Medium: FL

Large: DLBL

397
Q

t(14, 18)

A

FL; bcl2 over-expression

* Neoplastic small B cells p/w late adulthood and painless LAD

398
Q

Treatment for symptomatic follicular lymphoma

A

Low-dose CTX or Rituximab

399
Q

Complication FL

A

DLBL: p/w enlarging lymph node

400
Q

Lack of tingible body macrophages in germinal centers of follices: follicular hyperplasia or follicular lymphoma

A

Follicular lymphoma

* They indicate active apoptosis

401
Q

Expression of BCL2 follices: follicular hyperplasia or follicular lymphoma

A

Follicular lymphoma

402
Q

t(11,14)

A

Mantle cell lymphoma (immediately adjacent to follicle); Cyclin D1 [promotes G1/S] – phosphorylates

403
Q

Marginal zone lymphoma

A

MALToma

* Hashimotos, Sjogren’s, H. pylori

404
Q

Most lymph nodes don’t typically have marginal zones, thus marginal zone lymphoma is associated with…

A

Chronic inflammatory states

405
Q

BL of the jaw vs. abdomen

A

c-myc

  • Jaw = endemic
  • Abdomen = sporadic
406
Q

t(8,14)

A

c-myc oncogene in BL

407
Q

High mitotic rate and starry sky appearance on histology of lymph node

A

Burkitt’s lymphoma

408
Q

Most common form of NHL; clinically aggressive

A

DLBL

409
Q

Reed-Sternberg cells

A

Call in cytokines and drive the inflammatory response

  • CD 15, 30
  • Hodkins lymphoma
410
Q

Reed-Sternberg cell surface marker

A

CD15, 30

411
Q

Hodkin’s lymphoma subtypes

A

Nodular sclerosis: mediastinal mass in a young adult female
Lymphocyte rich (best pgx)
Mixed cellularity (IL-5, eosino)
Lymphocyte depleted: worst pgx (HIV)

412
Q

Mixed cellularity HL

A

IL-5 production by RS cells; eosinophilia

413
Q

Remnant of the mesonephric duct in the lateral vaginal wall.

A

Gartner duct cyst

414
Q

Prolactin inhibits the release of

A

GnRH

415
Q

GH adenoma: children vs. adults. What condition is usually present?

A

Children: gigantism
Adults: acromegaly
* 2 DM

416
Q

Most common cause of death in acromegaly

A

HF

417
Q

Lack of GH suppression with oral glucose is present in which pituitary disease?

A

Acromegaly

418
Q

Treatment of Acromegaly

A

Octreatide, GHR antag, surgery

419
Q

Common cause of hypopituitarism in a child

A

Craniopharyngioma

420
Q

Poor lactation and loss of pubic hair 2/2 pregnancy

A

Sheehan syndrome

421
Q

Central DI

A

2/2 ADH deficiency: hypothalamus or posterior pituitary

422
Q

Nephrogenic DI 2/2 what drug?

A

Lithium

423
Q

Hyponatremia, low serum osmolality, MS changes and seizures. Common causes

A

SIADH

  • SCLC
  • CNS trauma
  • Pulmonary infection
  • Drugs, i.e. cyclophosphamide
424
Q

Medical treatment of SIADH

A

Demclocycline

425
Q

Anterior neck mass; cystic dilation of thyrossal duct remnant

A

Thyroglossal duct cyst

426
Q

Persistence of thyroid tissue at the base of the tongue; P/W base of tongue mass

A

Lingual thyroid

427
Q

Differentiate between mechanism of increase in BMR vs. SNS activity in hyperthyroidism

A

BMR: Na-K ATPase
SNS: B1 adrenergic R

428
Q

Heat intolerance vs. Cold intolerance: Hyper/Hypo-thyroidism

A

Heat intolerance: Hyperthyroid

429
Q

T/F An elderly pt w hyperthyroidism can p/w afib

A

T

430
Q

Hyperthyroidism: cholesterol and sugar (increased or decresed)

A

Hypocholesterolemia, Hyperglycemia [GNG/Glycogenolysis]

431
Q

Pre-tibial myxedema & exopthalmos; explain the pathophysiology

A

Hyperthyroidism

* Fibroblasts with TSH R; secrete excess GAG’s

432
Q

Scalloping of thyroid follicle is classically present in which disease

A

Grave’s disease

433
Q

Thyroglobulin is derived from what AA?

A

Tyrosine

434
Q

Peroxidation involves (thyroid)

A

Oxidation, organification, coupling of TG w/ I

435
Q

Treatment of thyroid storm

A

PTU, beta-blockers, steroids

436
Q

Does PTU block peripheral conversion of T4 to T3?

A

Yes

437
Q

What is the classicaly cause of multi-nodular goiter?

A

Iodine deficiency

438
Q

Mental retardation, short stature with skeletal abnormalities, coarse facial features, enlarged tongue and umbilical hernia in a child

A

Cretinism 2/2 maternal hypothyroidism, thyroid agenesis, dyshormonogeneetic goiter, I deficiency

439
Q

The most important cause of dyshormonogenetic goiter.

A

Lack of TPO

440
Q

Another name for hypothyroidism in an adult

A

Myxedema: weight gain, slowing of mental activity, muscle weakness, cold intolerance with decreased sweating

441
Q

2 classic anatomic areas for myxedema in an adult

A

Larynx (deepening of voice)

Tongue (enlarged)

442
Q

Can Lithium case hypothyroidism?

A

Yes

443
Q

HLA-DR5

A

Hashimoto thyroiditis

444
Q

Which HLA is associated with Hashimoto thyroiditis?

A

HLA-DR5

445
Q

Anti-microsomal Ab

A

Hashimoto’s thyroiditis

[markers of damage, rather than mediators of disease]

446
Q

In what condition do you get chronic inflammation with germinal centers and Hurthle cells? Increased risk of marginal zone lymphoma?

A

Hypothyroidism (Hashimoto’s)

* Yes

447
Q

Young woman with a tender thyroid

A

Subacute deQuervain granulomatous thyroiditis

448
Q

Chronic inflammation with extensive fibrosis of thyroid that p/w hard-as-wood nontender thyroid. Complications?

A

Reidel Fibrosing Thyroiditis

* Involvement to local structures, i.e. airway

449
Q

Anaplastic thyroid ca vs. Reidel Fibrosing thyroiditis

A

Anaplastic: old people
Reidel: young people

450
Q

They key way by which you bx the thyroid

A

FNA

451
Q

Benign proliferation of thyroid follicles surrounded by fibrous capsule.

A

Thyroid follicular adenoma

452
Q

4 types of thyroid ca

A
  1. Papillary (LN, orphan Annie)
  2. Follicular (Blood)
  3. Medullary (calcitonin, MEN)
  4. Anaplastic
453
Q

Major risk factor for the most common type of thyroid carcinoma

A

Papillary / exposure to ionizing radiation in childhood [radiated for severe acne]

454
Q

Orphan Annie eyes with nuclear grooves & psammoma bodies

A

Papillary ca of thyroid

455
Q

T/F In both follicular adenoma and follicular carcinoma of the thyroid, the tumor is surrounded by a fibrous capsule.

A

True! (Ca obviously invades capsule)

456
Q

Can FNA be used to distinguish follicular adenoma from follicular carcinoma of the thyroid?

A

No

457
Q

The 4 carcinomas that tend to spread hematogenously

A
  1. RCC
  2. HCC
  3. FC thyroid
  4. Choriocarcinoma
458
Q

Calcitonin, amyloidosis: Thyroid cancer

A

MTC

459
Q

MEN 2A & B are associated with which oncogene?

A

RET

460
Q

3 major tissues that PTH acts on

A
  1. Kidney: PTH
  2. GIT: inc Ca and PO4
  3. Bone: clastic
461
Q

Does PTH act on osteoblasts or clasts?

A

!!Blasts!!: RANKL –> RANKR (clasts)

462
Q

Most common cause of primary hyperparathyroidism

A

PTH adenoma

463
Q

Osteitis fibrosis cystica is caused by

A

Hyperparathyroidism

464
Q

Increased or Decreased: Urinary cAMP & Alk Phos in hyperparathyroidism

A

Increased

465
Q

Is alk phos a sign of osteoblastic or clastic activity?

A

Blastic

466
Q

Most common cause of 2 hyperparathyroidism

A

Chronic renal failure

* Excess serum phosphate binds free Ca

467
Q

Alk phos in all hyperparathyroidism disorders is increased because

A

Increased osteoblastic activity

468
Q

Causes of hypoparathyroidism

A

AI damage, surgical excision, DiGeorge syndrome

469
Q

Trousseau sign vs. Chovstek sign

A

Chovstek: tapping facial n.
Trousseau: fill BP cuff, spasm

470
Q

AD disorder associate with short stature, short 4th and 5th digits, hypocalcemia with increased PTH levels

A

Pseudohypoparathyroidism

* End organ resistance to PTH (Gs)

471
Q

PTH is associated with Gs or Gq

A

Gs

472
Q

HLA-DR3 & DR4 in the context of islet cell inflammation

A

DM1

473
Q

Why does stress predispose a pt w/ DM1 to p/w DKA

A

Stress –> Epi –> Glucagon

474
Q

Treatment DKA

A

Fluids, insulin, K

475
Q

Amyloid deposition in islets

A

DM2

476
Q

NEG of large/medium vessels and small vessels in DM

A

Lg/Med: atherosclerosis

Small: hyaline

477
Q

Which cells in the body are particularly prone to osmotic damage? What is the key enzyme?

A

Schwann cells, pericytes of retinal blood vessels, lens

* Aldose reductase *

478
Q

Episodic hypoglycemia with MS changes relieved by glucose

A

Insulinoma

479
Q

ZES ulcers can extend into…

A

Treatment-resistant peptic ulcers; may be multiple and can extend into the jejunum

480
Q

Achlorhydria, cholelithiasis, steatorrhea

A

Somatostatinoma [gastrin/CCK]

481
Q

Watery diarrhea, hypokalemia, achlorhydria

A

VIPoma

482
Q

Adrenal hormones are derived from…

A

Cholesterol

483
Q

Why do you see muscle weakness with thin extremities in Cushing syndrome?

A

Muscle breakdown for GNG; storage for fat in face, neck, trunk

484
Q

Why do you see abdominal striae in Cushings?

A

Cortisol impairs synthesis of collagen

485
Q

Why do you see HTN in Cushing’s?

A

Cortisol increases alpha-1 R on arterioles

486
Q

Immune suppression in Cushing’s syndrome is mediated by:

A
  1. Inhibit PLA2
  2. Inhibit IL-2
  3. Inhibits histamine release
487
Q

Most common cause of Cushing syndrome

A

Excess CS: will shut down ACTH production and lead to atrophic adrenal glands

488
Q

2 difference cells aldosterone works on in the kidney

A
  1. Principal cell: dumps K

2. Alpha intercalated cell: dumps H+

489
Q

Most common cause of AR congenital adrenal hyperplasia

A

21-hydroxylase deficiency

* Clitoral enlargement in females/precocious puberty in males

490
Q

Acute adrenal insufficiency

A

Waterhouse-Friderichensen syndrome * sac of blood * [lack of cortisol]

491
Q

Chronic adrenal insufficiency

A
  1. AI destruction
  2. TB
  3. Mets (Lung ca)
492
Q

A high yield cause of hypotension, hyponatremia, hypovolemia, hyperkalemia, weakness, hyperpigmentation, vomiting, diarrhea. Where is the primary malignancy?

A

Chronic adrenal insufficiency

* Mets to adrenal from lung

493
Q

Why do you seen hyperpigmentation with excess ACTH?

A

POMC – > melanocyte stimulating hormone

494
Q

Color of pheo?

A

Brown

495
Q

10% rule of pheo

A

10% b/l, 10% familial, 10% malignant, 10% located outside of adrenal medulla [tihnk about wall of bladder]

496
Q

Several causes of pheo

A
  1. MEN2A, B
  2. VHL
  3. NF-1
497
Q

A ‘myelophthisic’ process that reduces normal hematopoiesis and leads to a peripheral ‘leukoerythroblastic’ picture with immature RBC’s and WBC’s in the peripheral blood, as seen here with nucleated RBCs and white cells even more immature than bands (metamyelocytes, myelocytes) on the smear

A

Metatstatic ca

498
Q

AD impaired cartilage proliferation in the growth plate due to activating mutation of…

A

FGFR3; AD, thought most mutations are new

499
Q

Short extremities with N size head and chest

A

Achondroplasia

500
Q

IM ossofication vs. EC ossification: Achondroplasia

A

Achondroplasia: long bone growth problems / problems with endochondral ossification [long bones, cartilage replaced]

501
Q

AD defect in collagen 1 synthesis

A

Osteogenesis imperfecta; multiple bone fractures, blue sclera and hearing loss [bones of ear]

502
Q

Why are sclera blue in OI?

A

Exposure of choriodal veins

503
Q

Inherited defect of bone resorption resulting in abnormally thick, heavy bone that fractures easily

A

Osteopetrosis

504
Q

The carbonic anhydrase II mutation can lead to what disease…

A

Osteopetoris: lack of acidic environment required for resorption of bone

[acid down pipes can remove calcium]

505
Q

Bone fractures, pancytopenia, vision/hearing loss, hydrocephalus and renal tubular acidosis

A

Osteopetrosis

506
Q

Treatment of osteopetoris

A

BMT (monocytes)

507
Q

Defective mineralization of osteoid

A

Rickets/Osteomalacia 2/2 low vitamin D

508
Q

Pigeon breast deformity, frontal bossing, rachitic rosary [costo-chondro junction deposition of osteoid] and bowing of legs in a child

A

Rickets

509
Q

Labs in osteomalacia, weak bones with increased risk for fracture

A

Decreased Ca, PO4

Increased PTH, ALP

510
Q

Alkaline phosphate creates an acidic/basic environment for osteoblastic activity

A

Basic environment

511
Q

Loss of trabecular bone mass that results in porous bone

A

Osteoporosis

512
Q

3 determinants of peak bone mass

A
  1. Diet
  2. Exercise
  3. Vitamin D receptor
513
Q

Is estrogen protective for bone mass?

A

Yes

514
Q

Bone pain and fractures in weight bearing areas; bone density low in DEXA scan; normal labs

A

Osteoporosis

515
Q

Treatment of osteoporosis

A

Exercise, vitamin D, ca, bisphosphonates, ERT, GC contraindicated

516
Q

Imabalance between osteoblastic and clastic function: viral etiology. Name the disease, its phases and its characteristic histology.

A

Paget’s disease of the bone

  1. Clastic
  2. Mixed
  3. Blastic
  4. Sclerotic
  • Cement lines / puzzle pieces / mosaic!
517
Q

Etiology of Paget’s disease

A

Possibly viral

518
Q

Isolated elevated ALP

A

Paget’s disease

519
Q

Treatment of early Paget’s disease

A

Calcitonin, bisphosphonates

520
Q

Complications of Paget’s disease

A

High output cardiac failure; osteosarcoma

521
Q

Infection of marrow space and bone; usually occurs in children. What part of the bone does it seed in kids vs. adults?

A
  • Osteomyelitis
    Kids: Metaphysis
    Adults: Epiphysis
522
Q

Name the parts of bone.

A

Distal to proximal: EMD

523
Q

Lytic focus of a bone surrounded by sclerosis on X-ray. How do you make the diagnosis?

A

Osteomyelitis

* Blood culture

524
Q

Ischemic necrosis of bone / bone marrow 2/2 trauma, fracture, steroids, SCD, Caisson disease (N-emboli)

A

Avascular, aspectic necrosis

525
Q

Classic example of Avascular, aspectic necrosis in bone of SCD patient

A

Dactylitis

526
Q

Benign tumor of bone that most commonly arisies on surface of facial bones; can be associated with Gardner syndrome

A

Osteoma

527
Q

Gardner syndrome

A
  1. FAB
  2. Neurofibromatosis retroperit
  3. Osteoma
528
Q

Benign tumor of osteoblasts surrounded by rim of reactive bone; occurs in young adults and arises in cortex of long bones

A

Osteoid osteoma

529
Q

Bone pain of osteoid osteoma is resolved with ___________. What does imaging reveal?

A

ASA; imaging reveals a bony mass w radiolucent (osteoid) core

530
Q

Bone pain similar to osteoid osteoma that does not resolve with ASA

A

Osteoblastoma (Arises in vertebreae); > 2cm

531
Q

Most common benign tumor of bone; tumor of bone with an overlying cartilage cap; arises from a lateral projection of growth plate

A

Osteochondroma

532
Q

Overyling cartilage of an osteochondroma can transform into…

A

Chondrosarcoma

533
Q

Malignant proliferation of osteoblasts; peak incidence in teenagers & elderly. Risk factors?

A

Osteosarcoma

* Familial Rb; Paget disease; radiation exposure

534
Q

Osteosarcoma arises in what part of bone?

A

Metaphysis of long bones; distal femur/proximal tibia

535
Q

Classic X-ray findings on osteosarcoma. Histology?

A

Drags periosteum off of the bone = Codman’s angle & hazy burst of sunlight
* Large pleomorphic cells producing pink osteoid

536
Q

Bone tumor in the epiphysis of long bones (usually distal femur or proximal tibia) with soap-bubble appearance on X-ray. Locally aggressive and may recur.

A

Giant cell tumor

537
Q

The only tumor that arises in the epiphysis of bone

A

Giant cell tumor

538
Q

Malignant proliferation of poorly-differentiated cells derived from…. Arises in the diaphysis of long bones in male children. Onion-skin appearance on X-ray

A

Ewing sarcoma

539
Q

X-ray appearance of bone tumor:

  1. Soap bubble
  2. Codman angle/rays of sun
  3. Onion-skin
A
  1. Soap bubble: Giant cell
  2. Codman angle/rays of sun: osteosarcoma
  3. Onion-skin: Ewing sarcoma
540
Q

Ewing sarcoma is a malignant proliferation of cells derived from

A

Neuroectoderm

541
Q

Small round blue cells of a bone tumor with tumor. Can resemble what conditions?

A

Ewing sarcoma = t(11,22)

  • Bone swelling & fever = osteomyelitis
  • Lymphoma
542
Q

t(11,22)

A

Ewing sarcoma

543
Q

Benign tumor of cartilage; usually arises in medulla of small bones of hand and feet. Malignant arises in the pelvis or skeleton

A

Chondroma vs. Chondrosarcoma

544
Q

Cartilage tumors usually arise in medulla or cortex of bones?

A

Medulla

545
Q

Usually, bone mets produce osteolytic, punched out lesions. The one exception is that produces osteoblastic lesions…

A

Prostate cancer classically produces osteoblastic lesions

546
Q

Describe the anatomy of a synovial joint

A

Bone, articular cartilage surrounded by joint capsule/synovium that secretes hyaluronic acid

547
Q

Degenerative joint disease

A

Progressive degeneration of articular cartilage; most often due to wear and tear. Additional risk factors (to age) include obesity and trauma

548
Q

DIP & PIP stiffness, hip, lower spine, knees that worsens during the day

A

Degenerative joint disease

549
Q

Eburnation of subchondral bone 2/2 disruption of articular cartilage with osteophyte formation (H+B nodes)

A

Osteoarthritis; Degenerative joint disease

550
Q

HLA-DR4

A

RA

551
Q

Synovitis leading to pannus

A

RA

* Inflammed granulation tissue. Leads to destruction of cartilage and ankylosis of joint

552
Q

Pathologic features of RA

A 
Ankylosis: fusion of joints
Joint deviation (myofibroblasts)
Disruption of cartilagel joint space narrowing, osteopenia

w/ fever, malaise, weight loss, myalgia

553
Q

Morning, symmetric stiffness that improves with activity

A

RA

554
Q

DIP is usually spared in: RA or OA?

A

RA

555
Q

Central necrosis surrounded by epithelioid histiocyte: what type of nodule?

A

Rheumatoid nodule

556
Q

Swelling of bursa behind the knee: OA or RA

A

RA

557
Q

Pleural effisions, LAD, interstitial lung fibrosis: RA or OA?

A

RA

558
Q

anti-Fc IgG IgM Ab

A

Rheumatoid factor

559
Q

Several complications of anklysoing spondylitis

A

Uveitis, aortitis [AR]

560
Q

Reiter syndrome

A

Arthritis, urethritis, conjunctivitis

* Young male weeks after GI or Chlamydia infection

561
Q

Sausage finger or toe associated with psoriasis

A

Psoriatic arthritis

562
Q

Infectious arthritis in an adult is caused by

A

N. gonorrohea

563
Q

2 mechanisms of gout

A

Increased production urate, poor excretion

564
Q

HGPRT responsible for

A

HX, G salvage [Lesch-Nyhann syndrome]

565
Q

Podagra

A

Painful arthritis of the great toe [gout]

566
Q

Why meat and ETOH can trigger gout?

A

Meat: DNA/RNA
ETOH: compete w/ urate at kidney

567
Q

Chronic gout manifestations

A

Tophi, renal failure

568
Q

Needle-shaped crystals with negative birefringence under polarized light

A
  • Gout
    Lay low = yellow
    Parallel light = yellow
569
Q

Pseudogout is 2/2 deposition of

A

Calcium pyrophosphate; rhomboid shaped crystals with weak + birefringence under polarized light

570
Q

Inflammation of skin and skeletal muscle of unknown etiology (could be associated with carcinoma, i.e. gastric)

A

Dermatomyositis

571
Q

Bilateral proximal muscle weakness [hair, stairs]; distal involvement; rash of upper eyelids [helioptrope], malar rash, red papules on elbows, knuckles and knees

A

Dermatomyositis

572
Q

Malar rash that is not SLE; ANA+, Anti-Jo-1 Ab +

A

Dermatomyositis

573
Q

Anti-Jo-1 Ab

A

Dermatomyositis

574
Q

Perimysial inflammation (CD4) vs. Endomysial inflammaion (CD8)

A

Dermatomyositis [closer to the skin] / Polymyositis

575
Q

Treatment of dermatomyositis

A

CS

576
Q

Replacement of skeletal muscle by adipose tissue occurs in

A

XLR MD

577
Q

The largest gene in the human genome

A

Dystrophin (anchors cytoskeletal to the ECM)

578
Q

Proximal muscle weakness at 1 year of age with elevated CK

A

DMD

579
Q

Death in DMD

A

Cardiac failure (or resp)

580
Q

What NMJ disorder is associated with Thymic hyperplasia/thymoma

A

MG

581
Q

Most common benign and malignant soft tissue tumor of adults. What is the characteristic cell in the malignant tumor?

A

Lipoma/Liposarcoma

*Lipoblast is characteristic cell

582
Q

Cardiac rhabdomyoma is associated with what syndrome?

A

Tuberous sclerosis

583
Q

Bening tumor of skeletal muscle

A

Rhabdomyoma

584
Q

Most common malignant soft tissue tumor in children [think young girl]. What is the positive stain?

A

Rhabdomyosarcoma; rhabdomyoblast that is desmin+; H+N (vagina in young girls)

585
Q

Derivates
Neural crest cells
Neural tube / wall
Lumen

A

PNS
CNS
Ventricles/SC canal

586
Q

T/F Anencephaly leads to maternal polyhydramnios

A

True [absence of CNS swallowing]

587
Q

Congenital stenosis of the channel that drains CSF from the 3rd to 4th ventricle

A

Cerebral aqueduct stenosis

588
Q

Lateral –> 3rd ventricle

A

Foramen of Monroe

589
Q

Congenital failure of the cerebellar vermis to develop. P/W massively dilated 4th ventricle with absent cerebelleum

A

Dandy-Walker Malformation

590
Q

Congenital extension of cerebellar tonsils through Foramen Magnum

A

Arnold Chiari Malformation
Type 1: no symptoms
Type 2: hydrocephalus
* Meningomyelocele; syringomyelia

591
Q

Cystic degeneration of the spinal cord; arises with trauma or Arnold-Chiari malformation. What level and what sensory loss?

A

Syringomyelia; C8-T1. Loss of pain and temperature [knocking out of anterior commissure]; also LMN +/- lateral horn

592
Q

Sympathetic innervation to the face and its spinal cord association

A

Lateral horn of T1

593
Q

Damage to the anterior motor horn 2/2 infection. LMN signs.

A

Poliomyelitis

594
Q

Inherited degeneration of anterior motor horn. Inheritance pattern and disease

A

AR; floppy baby [Werdnig Hoffmann disease]

595
Q

Degenerative disorder of upper and lower motor neurons (CS tract)

A

ALS
Anterior: LMN signs
Lateral CS: UMN signs

596
Q

What distinguishes ALS from syringomyelia?

A

Lack of sensory impairment in ALS

597
Q

What is the earliest sign of ALS?

A

Atrophy and weakness of hands

598
Q

In familial cases of ALS, what mutation is present?

A

Zn-Cu SOD mutation

599
Q

Degenerative disorder of cerebellum and spinal cord tracts; P/W ataxia w/ loss of vibration/proprioception, muscle weakness in LE and loss of DTR

A

Freidreich Ataxia

* GAA frataxin gene [cannot regulate Fe properly]

600
Q

What is the underlying pathophysiology in Friedreich Ataxia?

A

AR unstable GAA repeat in frataxin gene; inability to properly regulate Fe

601
Q

What is the disease associated with Freidreich Ataxia?

A

Hypertrophic CM

602
Q

Leptomeninges consist of

A

Pia and arachnoid

603
Q

Meningitis in neonates

A

GBS, E. coli, L. monocytogenes

604
Q

Meningitis in children/teenagers

A

N. m

605
Q

Meningitis in adults and elderly

A

S. pna

606
Q

Meningitis in nonvaccinated infants

A

H. flu

607
Q

What is the route of transmission of N. m?

A

Nasopharyngeal

608
Q

What level do you do an LP?

A

L4-L5: level of iliac crest

609
Q

Spinal cord ends at

A

L2

610
Q

Normal glucose is approximately what percentage of serum glucose?

A

66%

611
Q

Complications of bacterial meningitis

A

Death, hydrocephalus, hearing loss, seizures

612
Q

Etiology of cerebrovascular disease

A

85% ischemia (focal, global)

15% hemorrhage

613
Q

Global cerebral ischemia etiology

A

Low perfusion (atherosclerosis), shock, chronic hypoxia (anemia), repeated hypoglycemia (insulinoma)

  • Mild
  • Moderate: infarcts in watershed areas
  • Severe
614
Q

Describe mild, moderate and severe global cerebral ischemia

A

Mild: insulinoma
Moderate: infarcts in watershed areas
Severe: death

615
Q

What histological layers of the brain are most susceptible to damage during global ischemia?

A
  • End of ACA, MCA
  • Pyramidal neurons of the cortex layers 3, 5, 6 = Cortical laminar necrosis
  • Pyramidal neurons of hippocampus
  • Purkinje layer of cerebellum
616
Q

What is cortical laminar necrosis?

A

Areas of the brain most susceptible to damage during decreased perfusion: layers 3, 5, 6 of cortex (also pyramidal neurons of the hippocampus)

617
Q

Focal ischemia of the brain results in…

A

Stroke (<24 h = TIA)

618
Q

3 ways to develop an ischemic stroke

A
  1. Thrombotic [pale at periphery of cortex]
  2. Embolic [red]
  3. Lacunar [hyaline arteriolosclerosis – most commonly involves the lenticulostriate vessels]
619
Q

Lacunar stroke

A

Ischemic stroke 2/2 hyaline arteriolosclerosis most commonly involves the lenticulostriate vessels

620
Q

Lenticulostriate vessels arise from and supply the…

A

MCA / deep structures of the brain

621
Q

Ischemic stroke leads to what type of necrosis?

A

Liquefactive; red neurons are early finding; PMN/microglial/granulation tx; results in a fluid-filled cystic space surroudned by gliosis

622
Q

What is the earliest change (histologically) in an ischemic stroke?

A

Red/pink neurons [12-24 hours]

623
Q

What are the 2 types of cerebral hemorrhage?

A
  1. Intracerebral

2. SA

624
Q

Intracerebral hemorrhage is classisically 2/2

A

Rupture of Charcot-Bouchard microaneurysm as a complication of HTN; basal ganglia is the most common site

625
Q

Charcot-Bouchard microaneurysm p/w

A

HA, nausea, vomiting, coma

626
Q

LP with xanthochromia

A

SA hemorrhage

627
Q

Most frequent cause of SA hemorrhage

A

Rupture of berry aneurysm; thin-walled saccular outpouching that lacks a media layer; most often located in anterior circle of Willis

628
Q

What layer of a blood vessel’s wall is absent in a berry aneurysm?

A

Media

629
Q

Lucid interval is seen in…

A

Epdural hematoma

630
Q

Lethal complication of epidural hematoma

A

Brain herniation

631
Q

Lethal complication of subdural hematoma

A

Brain herniation

632
Q

Tonsillar herniation

A

Herniation of cerebellar tonsils through FM –> CP arrest

633
Q

Subfacline herniation

A

Cingulate gyrus herniates under falx –> compress the ACA

634
Q

Uncal herniation

A

Uncus of temporal lobe; CN 3, PCA, Duret hemorrhages

635
Q

Duret hemorrhages

A

Consequence of uncal herniation

636
Q

Inherited mutation in ezymes necessary for production or maintenance of myelin

A

Leukodystrophy

637
Q

Deficiency of arylsulfatase; myelin cannot be degraded and thus accumulates in lysosomes

A

Metachromatic leukodystrophy

638
Q

Deficiency of galactocerebroside B- galactosidase

A

Krabbe disease

639
Q

Impaired addition of coenzyme A to LCFA; fatty acids accumulate damaging adrenal gland and white matter

A

Adrenoleukodystrophy

640
Q

HLA DR-2

A

MS

641
Q

AI destruction of CNS myelin and oligodendrocyte; seen in regions away from the equator

A

MS

642
Q

Blurred vision in one eye, vertigo/scanning speech and internuclear opthalmoplegia

A

MLF

643
Q

LP with lymphocytes, Ig with oligoclonal IgG bands and myelin basic protein

A

MS

644
Q

Acute attack of MS treated with vs. LTM

A

Acute: high dose steroids
LTM: IFN-beta

645
Q

Progressive, debilitating encephalitis leading to death. Due to slowly progressing, persistent infection of brain by what virus?

A

Mealses; SSPE

* Viral inclusions in gray /white matter

646
Q

JC infection of oligodendrocytes p/w rapidly progressing neurology and death

A

PML; IS leads to reactivation of latent virus

647
Q

PML vs. SSPE

A

SSPE: Measles [white and gray]
PML: JC virus

648
Q

Focal demyelination of the pons that p/w locked in syndrome

A

Central pontine myelinosis; due to rapid IV correction of hyponatremia

649
Q

Degeneration of gray neurons in cortex vs. basal ganglia

A

Cortex: dementia

Basal ganglia: gray matter

650
Q

Degenerative disease of the cortex

A

Alzheimer disease

651
Q

APP receptor broken down to a beta product which is then deposited as… [in the brain]

A

AB amyloid

652
Q

Major risk factor for sporadic Alzheimer’s is…

A

Age, APOE4

653
Q

APOE4 vs. APOE2 and Alzheimer’s risk

A

APOE4: higher number/increased risk
APOE2: lower/decreased risk

654
Q

Early onset Alzheimer’s a/w

A
  1. Pre-synelin 1 [mutation] & 2

2. Down’ syndrome [APP on Ch. 21]

655
Q

Presenilin 1 mutation

A

Alzheimers

656
Q

Gross specimen of an Alzheimer’s brain

A

Diffuse cerebral atrophy, narrowing of gyri, widening of sulci
* Hydrocephalus ex vacuo [atrophy of brain 2/2 loss of parenchyma]

657
Q

Hydrocephalus ex vacuo

A

[atrophy of brain 2/2 loss of parenchyma]

* Alzheimer’s

658
Q

A neuritic plaque in Alzheimer’s

A
  1. AB amyloid (from APP)
    - -can deposit around BV/cerebral amyloid amylopathy
  2. Neuritic processes
659
Q

NF tangles are seen in…

A

Alzhemier’s: intracellular / tau proteins (MTOC proteins)

660
Q

Hyperphosphorylated tau proteins

A

Microtubular associated protein seen in intracellular accunulations in Alzheimers [hyperphosphorylated]

661
Q

Multifocal infarction and injury 2/2 HTN, atherosclosis, or vasculitis

A

Vascular dementia

662
Q

Degenerative disease of frontal and temporal cortex

A 
Pick disease (tau protein aggrgates)
* Behavior and language
663
Q

NF tangles vs. round aggregates of tau proteins

A

Tangles: Alzheimer’s
Round: Pick disease

664
Q

The striatum receives input from

A

Cortex and SN pars compacta; can send stimulatory or inhibitory signals to the cortex

665
Q

D1 vs. D2 receptors

A

D1: increase stimulation
D2: decrease inhibition

666
Q

Rare exposure to MPTP in drugs can lead to what disease?

A

Parkinson’s disease

667
Q

Lewy bodys

A

Parkinson’s [composed of alpha synuclein]

668
Q

Synuclein vs. Sineilin

A

Synuclein: Parkinson’s
Sinelin: Alzheimer’s

669
Q

Early-onset dementia in Parkinson’s = (vs. late onset)

A

Lewy body dementia

670
Q

Degeneration of GABAeric neurons in the caudate nucleus of the basal ganglia

A

Huntington disease

671
Q

The striatum is composed of

A

Caudate & Putamen

672
Q

GABA is a stimulatory/inhibitory NT

A

Inhibitory (GABAeric neurons and Huntington’s disease)

673
Q

What structures sit just laterally to the lateral ventricles?

A

Striatum (caudate—-IC—-putamen)

674
Q

Anticipation is due to…

A

Further expansion of the trinucleotide repeat during spermatogenesis

675
Q

Chorea, athetosis, demention, depression, suicide

A

Huntington’s disease

676
Q

Increased CSF that leads to dilated ventricles

A

NPH; can cause dementia in adults; LP releives symptoms

677
Q

NPH vs. Hydrocephalus ex. vacuo

A

NPH:

Ex vacuo:

678
Q

NPH triad

A

Dementia, gait instability, urinary incontinence [wet, wacky, wobbly]

679
Q

The nerve fibers running along the ventricles

A

Corona radiata

680
Q

Treatment of wet, wobbly, wacky disorder?

A

LP/shunt [NPH]

681
Q

Arachnoid granulations

A

Drain the CSF

682
Q

Degenrative disease 2/2 prion protein

A

Spongiofrm encephalopathy

683
Q

PrP –> PrP SC

A

Beta-pleated sheet

  • Pathologic / cannot degrade
  • Spongy holes in white gray matter [intracellular vaculoes]
684
Q

Etiology of spongiform encephalopathy

A
  1. Sporadic
  2. Inherited
  3. Transmitted
685
Q

CJD is usually sporadic; but can arise due to exposure to prion infected human tissue

A

Human growth hormone; corneal transplant

* P/W rapidly progressive dementia a/w ataxian and startle myoclonus; spike-wave complexes seen on EEG

686
Q

Spike-wave complexes on EEG

A

CJD

687
Q

vCJD is related to exposure to…

A

Bovine spongiform encephalopathy (mad cow disease)

688
Q

Familial fatal insomnia

A

Inherited form of prion disease characterized by insomnia and exaggerated startle response

689
Q

What 3 cancers classically metastasize to the brain?

A

Lung, breast, kidney

690
Q

What cells in the brain form the blood brain barrier?

A

Astrocytes

691
Q

Malignant high grade tumor of astrocytes; most common malignant CNS tumor in adults

A

GBM; crosses corpus collosum

692
Q

GBM histologic hallmarks & IHC marker

A
  1. Large amount of necrosis
  2. Edge of necrosis/ pseudopallasading
  3. Endothelial cell proliferation
  • GFAP + (derived from glial cell)
693
Q

Most common benign brain tumor in adults

A
  • Meningoma

Benign tumor of arachnoid cells; F>M; p/w seizure.

694
Q

What receptor is expressed by meningioma brain tumor?

A

Estrogen receptor

695
Q

Benign brain tumor with wholrled cells & psammoma bodies

A

Meningioma

696
Q

Benign tumor of Schwann cells; IHC marker

A

Schwannoma, S100+, B/L NF-2

697
Q

S100+ brain tumor

A

Schwannoma

698
Q

Calcifed tumor in white matter of frontal lobe p/w seizure

A

Oligodendroglioma; malignant

699
Q

Histology of oligodendroma

A

Fried egg

700
Q

Most common brain tumor of chidlren p/w cyst + neural nodule on MRI

A

Pilocytic astrocytoma (benign)

701
Q

Histologic hallmark of pilocytic astrocytoma

A

Rosenthal fibers

702
Q

Malignat tumor derived from the granular cells of the cerebullum. Histology

A

Medulloblastoma [neuroectoderm]

* Arises in children; small, round blue cells w/ Homer-Wright rosettes. Poor pgx

703
Q

Homer-Wright rosettes vs. Rosenthal fibers

A

HW: Medulloblastoma
Rosenthal: pilocytic astrocytoma

704
Q

T/F A medulloblastoma grows rapidly, spreads via CSF and can p/w drop mets

A

T

705
Q

Malignant brain tumor of children. Most commonly arises in the 4th ventricle; may p/w hydrocephalus

A

Ependymona

706
Q

Homer-Wright rosettes vs. Perivascular pseudo-rosettes vs. Rosenthal fibers

A

Homer W: Medulloblastoma
Perivascuar pseudorosettes: Ependymoma
Rosenthal fibers: pilocytic astrocytoma

707
Q

Tumor that arises from he epithelial remnants of Rathke’s piouch

A

Carniopharyngioma

708
Q

Upward protrusion of the floor of the mouth

A

Rathke’s pouch = AP

709
Q

T/F Craniopharyngioma is calcified on imaging

A

True

710
Q

Hypospadias

A

Opening of the urethra on the inferior surface of the penis (ventral)
* Failure of the urethral folds to close

711
Q

Epispadias

A

Opening of the urethra on the superior surface of the penis 2/2 abnormal positioning of the genital tubercle
* A/W Bladder extrosphy

712
Q

Epispadias is a/w

A

Bladder extrosphy

713
Q

Condyloma acuminatium

A

Benign warty growth on genital skin 2/2 HPV 6, 11 characterized by koilocytic change [raisin like nuclei]

714
Q

Necrotizing granulomatous inflammation of inguinal lymphatics and lymph nodes

A

Chlamydia trachomatis [OIC]

* Heals w fibrosis and perianal involvement may result in rectal strictures.

715
Q

LGV vs. chancroid vs. condyloma lata vs. condyloma accuminatum

A

LGV: C. trachomatis
Chancroid: H. ducreyi
CL: Syphillis
CA: HPV

716
Q

Chlamydia serotypes

A

A-c: trachoma
D-k: UG + conjunvtivitis
L1-L3: LGV

717
Q

Risk factors for SCC penis

A

High risk HPV (2/3); lack of circumcision

718
Q

Precursor lesions to SCC penis

A

Bowen disease: shaft
Erythroplasia of queyrat: glans
Bowenoid papulosis: reddish papules

719
Q

Bowen disease

A

Precursor lesions to SCC penis (shaft); in situ carcinoma – leukoplakia

720
Q

Erythroplasia of Queyrat

A

Precursor lesions to SCC (glans) penis – erythroplakia

721
Q

Bowenoid papulosis

A

Precursor lesions to SCC penis (reddish papules)

722
Q

Failure of testicle to descend into the scrotal sac

A

Cryptoorchidism

723
Q

1 congenital male reproductive abnormality

A

Cryptoorchidism

724
Q

Complications of cryptoorchidism

A

Testicular atrophy w/ infertility [lower temperature] and increased risk for seminoma

725
Q

Orchitis 2/2

A

Chlamydia D-K, Neisseria, E. coli, Pseudomonas, Mumps, AI

726
Q

Hallmark of AI orchitis

A

Tubular granulomas (non nex)

727
Q

Twisting of spermatic cord; leads to hemorrhagic infarction 2/2 congenital failure of testes to attach to inner lining of scrotum

A

Testicular torsion

728
Q

Adolescent with sudden onset testicular pain and absent cremasteric reflex

A

Testicular torsion

729
Q

Dilation of spermatic vein 2/2 impaired drainage. P/W scrotal swelling with bag of owrms appearance

A

Varicocele; usually left-sided with L- RCC

730
Q

T/F Varicocele is seen in a large percentage of infertile males

A

T

731
Q

Fluid collection within the tunica vaginalis; a/w incomplete closure of processus vaginalis (infants) or blocakge of lymphatic drainage (adults); transillumination +

A

Hydrocele

732
Q

2 types of testicular tumors

A
  1. Germ cell

2. Sec-cord stroma

733
Q

Are testicular tumors biopsied?

A

No – risk of seeding scrotum; must be removed via radical irchiectomy

734
Q

> 95% of testicular tumors are categorized …

Risk factors

A

Germ cell tumor; ages 15-40

  • Risk factors = cryptochidism and Klinefelter syndrome
  • Divided into seminoma & non-seminoma
735
Q

Dysgerminoma in the ovary. _____________ in the testes

A

Seminoma

736
Q

Seminoma vs. Non-seminoma: Responds to radiation, metastazies late and has an excellent prognosis

A

Seminoma

737
Q

Seminoma vs. Non-seminoma: Poor/variable response to treatment and metastazies early

A

Non-seminoma

738
Q

Can rare cases of seminomas produce beta-HCG?

A

Yes

739
Q

Homogenous malignant tumor of testicle with no hemorrhage or necrosis

A

Seminoma [lg cells with clear cytoplasm]

740
Q

Malignant testicular tumor of immature, primtive cells that may form glands; hemorrhage w nex; agressive; CTX can result in differentiation [i.e. a teratoma]. Increased AFP/beta-HCG

A

Embryonal carinoma

741
Q

Relief of pain with lifting tests

A

Positive Prenh sign: epididymitis (vs. torsion)

742
Q

Can embryonal ca of testes form glands?

A

Yes

743
Q

Most common testicular tumor in children. Serum marker? Histology?

A

Yolk sac tumor; AFP positive

* Schiller Duvall body

744
Q

What can male chioriocarcinoma lead to? Why?

A

Hyperthyroidism or gynecomastia (alpha subunit of beta-HCG is similar to FSH, LH, TSH)

745
Q

What is the one cancer (classically) that p/w a tiny primary, but massive secondaries?

A

Choriocarcinoma

746
Q

Teratoma is benign or malignant in males?

A

Malignant

747
Q

T/F Most male germ cell tumors are mixed.

A

T

748
Q

Sex cord stomal tumors of testes

A

Leydig cell: androgen [Reinke cell crystals]

Sertoli cell: tubules

749
Q

Most common cause of testicular mass in males over 60

A

Lymphoma; often B/L & usually DLBL

750
Q

Acute prostatitis in young vs. old males

A

Young: C/Ng
Old: E coli, Pseudomonas

751
Q

BPH is related to what hormone?

A

DHT

752
Q

BPH occurs in what zone of the prostate?

A

Periuretheral

753
Q

Treatment of BPH

A

Prazosin (alpha-antag), Tamsulosin; 5-alpha-reductase inhibitor

754
Q

Risk factors for prostate AC

A

Age, race (AA vs. Asians), diet high in saturated fats

755
Q

Most common location for prosate AC

A

Posterior periphery

756
Q

Decreased % of free PSA in the serum

A

Suggestive of PRCA. Cancer makes bound PSA

757
Q

T/F Nuclei contain dark nucleoli in PRCA

A

True

758
Q

Gleason grading is based on architecture or nuclear atypia

A

Archictecture

759
Q

Low back pain with increased ALP, PSA, PAP

A

PRCA (osteoblastic mets)

760
Q

PRCA local disease treatment

A

Prostatectomy

761
Q

Continuous GnRH analog used to treat PRCA

A

Leuprolide

762
Q

Androgen receptor inhibitor used to treat PRCA

A

Flutamide

763
Q

Type I HSR of the skin a/w asthma and allergic rhinitis

A 
Atopic dermatitis (Eczema)
* Pruritic, erythematous, oozing rash with vesicles and edema
764
Q

Ezema usually involes

A

The face & flexor surfaces

765
Q

Contact dermatitis irritants

A

Poson ivy, nickel (type 4 HS), detergents, drugs (PCN)

766
Q

Comedones, pustules, nodules

A

Acne (Comedone = white/blackhead)

767
Q

The pathophysiology of Acne

A

Excess sebum & keratin; P. acnes /lipases break down sebuml inflammation leads to pimples

768
Q

What skin condition can isotretinoin be used for?

A

Acne (vitamin A derivative)

* Decereases keratin production

769
Q

Well-circumscribed salmon-colored plaques with a silvery scale on extensor surfaces and scalp with pitting of nails

A

Psoriasis

770
Q

HLA-C

A

Psoriasis

771
Q

Psoriasis is 2/2

A

Excessive keratinocyte proliferation [ often in an area of trauma]

772
Q

Acanthosis

A

Excessive epidermis

773
Q

Parakeratosis

A

Nucleated keratinocytes

774
Q

Monroe microabscesses

A

Collection of PMN’s in the S. corneum (psoriasis)

775
Q

Elongation of dermal papillae contributes to what sign seen in psoriasis?

A

Psoriasis

* Pinpoint bleeding = Auspitz sign

776
Q

PUVA treatment for what skin condition?

A

Psoriasis (psoralen + UVA light)

777
Q

Pruritic, planar, polygonal, purple papules w/ reticular white lines on surface (Wickham striae) involving wrists, elbows and oral mucosa

A

Lichen planus

778
Q

Inflammation at the dermal-epidermal junction is seen in what skin disorder? Saw-tooth appearance

A

Lichen planus

779
Q

Lichen planus is associated with what virus?

A

HCV

780
Q

Anti-desmoglein IgG

A

PV

781
Q

Acantholysis

A

Separation of keratinocytes

782
Q

Oral mucosa: PV or BP

A

PV

783
Q

Blisters that rupture easily vs. those that don’t rupture easily

A

Easily: PV

Not easily: BP

784
Q

AI deposition of IgA at the tips of dermal papillae that pw/ pruritic vesicles and bullae that are grouped

A

Dermatitis herpetiformis [celiac disease cross-reactive Ab]

785
Q

HSR with targetoid rash and bullae; most commonly seen with HSV, but can be seen w infections, i.e. mycoplasma, PCN, SLE, malignancy

A

Erythema multiforme

786
Q

Erythema multiforme with oral mucosa involvement and fever. What is the most severe form called?

A

SJS; TEN (2/2 ADR)

787
Q

Benign proliferation of squamous cells in the skin p/w pseudocyts on histology and a raised, stuck on lesion; common in the elderly

A

Seborrheic keratosis [raised discolored, stuck on]

788
Q

Leser-Trelat sign

A

Sudden onset multiple seborrheic keratoses; suggests and underlying carcinoma of GIT

789
Q

Epidermal hyperplasia with darkening of skin (velvet-like); involves the groin/axilla; associated with insulin resistance or malignancy (gastric ca)

A

Acanthosis nigricans

790
Q

Risk factors squamous and basal cell ca

A

Prolonged exposure to sunlight, albinism, xeroderma pigmentosum

791
Q

UV- A, B, or C is most dangerous

A

UV-B

792
Q

Xeroderma pigmentosum

A

AR: nucleotide excision repair pathway

[thymidine dimers]

793
Q

Which skin cancer is surrounded by teleangectasias (w peripheral palisading)? Where is the most classic location?

A

Basal cell ca; upper lip

794
Q

Additional risk factors for SCC skin

A

IS therapy, arsenic poisoning, chronic inflammation (scar from burn or draining sinus tract)

795
Q

Upper lip vs. lower lip skin cancer

A

Upper: Basal
Lower: Squamous

796
Q

Precursor to squamous cell carcinoma of the skin; p/w hyperkeratotic, scaly plaque on face, back or neck

A

Actinic keratosis

797
Q

Very well-differentiated SCC of skin; develop rapidly and regresses spontaneously; presents as a cup-shaped tumor filled with keratin debris

A

Keratoacanthoma

798
Q

Melanocytes are dervied from

A

Neural crest

799
Q

Melain is synthesized in what organelle?

A

Melanosomes –> passed to keratinocytes

800
Q

AI destruction of melanocytes

A

Vitiligo (localzied loss of skin pigmentation)

801
Q

What enzyme defect in albinism?

A

Tyrosinase

802
Q

What are freckles?

A

Small, tan-brown macules; darkens when expsed to sunlight; due to increased numbers of melanosomes

803
Q

Mask like hyperpigmentation of cheeks A/W pregnancy and OCP

A

Melasma

804
Q

Benign neoplasm of melanocytes

A

Nevus (congenital p/w hair)

805
Q

Nevus vs. melanoma

A

Nevus: has hair growing from it

806
Q

Junctional nevus

A

Grows along the dermal-epidermal junction [children]

807
Q

Compound nevus

A

Nevus that grows down into the dermis

808
Q

Intradermal nevus

A

Most common in adults

809
Q

Junvtional vs. Intradermal nevus

A

Junctional: children
Intradermal: adults

810
Q

Inheritance: Dysplastic nevi that may progress to melanoma

A

Dysplastic nevus syndrome: AD

811
Q

Growth phases of melanoma & most important feature for mets

A
  1. Radial (horizontally) – low risk mets

2. Vertical (key feature for mets)

812
Q

Subtypes of melanoma (4)

A
  1. Lentigo (radial - good pgx)
  2. Superficial spreading (radial - good pgx)
  3. Nodular (early vertical - poor pgx)
  4. Acral lentigionus: palms/soles in dark-skinned individuals; not related to UV light exposure
813
Q

Superficial bacterial skin infection 2/2 S. aureus or S. pyogenes p/w erythematous macules that progress to pustules on face (honey-colored serum)

A

Impetigo

814
Q

Deeper dermal infection 2/2 S. aureus or S. pyogenes p/w/ red, tender, swollen rash with fever

A

Cellulitis (surgery, trauma, insect bite)

815
Q

Necrosis of SC tissue 2/2 anaerobic flesh eating bacteria

A

Necrotizing fasciitis: CO2/crepitus

816
Q

Sloughing of skin with erythematous rash and fever

A

Staph Scalded Skin Syndrome [epidermolysis of s. granulosum / exfoliative A & B toxin]

817
Q

SSS vs. TEN

A

SSS: S. granulosum
TEN: DEJ

818
Q

Verruca on hand/feet is 2/2

A

Wart: flesh-colored papule with rough surface 2/2 HPV infection of keratinocytes

819
Q

Firm, pink umbilicated papules 2/2 pox virus [bodies = inclusions]

A

Molluscum contagiousm

Step 1 Prep (15 decks)

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