Brainscape's Knowledge GenomeTM

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


See full index

Path 404 > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Benign Breast Pathologies (4)

A
  • Acute Mastitis
  • Duct Ecstasia
  • Fibroadenoma
  • Fibrocystic Change
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Acute Mastitis: Epidemiology

A
  • occurs almost exclusively in lactating women

- usually in first several months post partum

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

Acute Mastitis: Pathogenesis

A
  • Occurs in presence of milk stasis which happens with obstruction of a milk duct… this leads to engorgement and potentially the release of milk into the surrounding breast tissue which induces an inflammatory response
  • may allow for infection (staph aureus or streptococcus)
  • can also develop without milk stasis when bacteria enters through cracked/damaged nipples.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Acute Mastitis: Clinical Presentation

A
  • pain/tenderness, swelling, redness, and warmth of breast

- low grade fever and malaise

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

Acute Mastitis: Treatment

A
  • drainage of milk from the breast

- warm compress, rest, and antibiotics if necessary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Is it safe for the baby to drink the milk of acute mastitis?

A
  • yes, gastric juices of infant’s stomach kill infectious agents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Duct Ecstasia: Pathogenesis

A
  • large ducts near the nipple become dilated (ecstatic)

- at least some cases appear to be related to degenerative changes of the duct wall

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

Duct Ecstasia: Epidemiology

A
  • usually occurs in older, multiparous women
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Duct Ecstasia: Clinical Presentation

A
  • nipple discharge (white), and sometimes nipple retraction

- fibrosis may develop around the dilated ducts and mimic carcinoma

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

Duct Ecstasia: Microscopic Findings

A
  • chronic inflammation and dilated ducts filled with macrophages and debris
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Duct Ecstasia: Treatment

A
  • if no mass legion, no treatment is necessary

- is mass is present, excision may be done to exclude carcinoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Fibroadenoma

A
  • Benign tumors of the breast that are composed of proliferating stromal and epithelial cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Fibroadenoma: Epidemiology

A
  • Usually occur in women in their 20s and 30s
  • can be multiple and/or bilateral
  • most common benign tumor in the breast
  • ~10% of women
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Fibroadenoma: Pathogenesis

A
  • thought to occur in response to estrogen stimulation of the tissue
  • polyclonal proliferation of cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Fibroadenoma: Clinical Presentation

A
  • mobile, round mass, ranging from 1cm to 4cm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Fibroadenoma: Microscopic Findings

A
  • well-circumscribed, round legions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Fibroadenoma: Treatment

A
  • some may not need treatment, others are removed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Fibrocystic Change

A
  • umbrella term

- encompasses numerous benign changes in the breast

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

Fibrocystic Change: Epidemiology

A
  • occurs most commonly in premenopausal women,but can occur in older women as well
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Fibrocystic Change: Clinical Presentation

A
  • can mimic clinical signs of BC like mass formation, mammographic calcification, other mammogram abnormalities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Fibrocystic Change: 3 histologic changes

A
  • ranked according to severity
  • Non-Proliferative
  • Proliferative (ductal hyperplasia) (1.5-2x the risk of BC)
  • Atypical Proliferative (4-5x the risk of BC)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Fibrocystic Change: Treatment

A
  • no treatment required, biopsy may be performed to rule out cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Breast Cancer risk factors (5)

A
  • Gender (F: 12% lifetime risk, M: 0.11% risk)
  • Age (risk increases with age, average age 61)
  • Genetic Factors (family history, BRCA1/2) (genetic is 3% of all BC)
  • Estrogen Exposure (high levels of estrogen increase risk)
  • Radiation Exposure (therapeutic doses)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

BC: Incidence and Mortality

A
  • 2nd leading cause of cancer death in US
  • incidence rose in early 80s (better screening), has leveled off
  • mortality declining since 1990s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

In Situ Carcinoma

A
  • Ductal Carcinoma In Situ, or DCIS
  • not invasive into surrounding tissue where lymph vessels are (not metastatic)
  • often diagnosed with mammogram
  • can be a precursor lesion to invasive carcinoma (8-12x higher risk)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Invasive Carcinoma

A
  • cancerous cells spread beyond the ducts into the lymphatic channels where it can metastasize
  • usually forms a mass legion
  • can sometimes be considered a “chronic disease” instead of a “terminal disease” b/c women can live many years with it
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Invasive Carcinoma: Clinical Presentations (6)

A
  • palpable lump
  • single mass
  • hard
  • immobile (advanced BC)
  • irregular borders (vs. smooth)
  • > 2 cm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Invasive Carcinoma: Diagnosis

A
  • biopsy, esp needle core biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Invasive Carcinoma: Prognostic factor - Stage guidelines

A
  • Tumor Size
  • Lymphatic Spread (can still be cured)
  • Distant Metastasis (generally incurable)
  • higher stage worse prognosis (Stage 0: 92% survival, stage IV: 13% survival)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Invasive Carcinoma: Common sites of metastisis

A
  • Axillary lymph nodes (almost always first, curable)
  • Distant Metastasis
  • Lungs
  • Bones
  • Liver
  • Adrenals
  • Brain, meninges, CSF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Invasive Carcinoma: Prognostic factor - Grade guidelines

A
  • assigned according to how abnormal the cells look under the microscope
  • not as powerful of a predictor of prognosis as stage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Invasive Carcinoma: Treatments (4)

A
  • Surgery
  • Radiation Therapy
  • Hormonal Therapy
  • Chemotherapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Invasive Carcinoma: Surgery types (4)

A
  • lumpectomy (only diseased tissue taken)
  • mastectomy (can also have with reconstruction)
  • Lymph node biopsy
  • lymph node dissection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Invasive Carcinoma: Hormonal Therapy

A
  • > 50% of BC express estrogen and progesterone receptors
  • often responsive to anti-estrogen agents (tamoxifen/aromatase inhibitors)
  • fewer and less severe side effects
  • sometimes used as preventive therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Invasive Carcinoma: Chemotherapy

A
  • Traditional (attack all rapidly proliferating cells)

- Targeted (antibody designed to attack cells that over-express HER2/neu

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Common non-neoplastic gynecological conditions (4)

A
  • STIs
  • Dysfunctional Uterine Bleeding
  • Endometriosis
  • Obstetric Conditions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Dysfunctional Uterine Bleeding

A
  • excessive menstruation or bleeding between periods
  • abnormality in the hypothalamic/pituitary/ovarian hormone mechanism
  • often peri-menopausal or right at menarche
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Excessive Menstruation

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

Bleeding between periods

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

Endometriosis

A
  • “powder burn”, “chocolate cyst,” old blood
  • presence of endometrial glands and stroma outside the uterus
  • common (~10% women in 20s and 30s)
  • frequently occurs in ovaries, fallopian tubes, pelvic peritoneum
  • symptoms include pain, adhesions, and infertility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Endometriosis Theories of Pathogenesis

A
  • retrograde menstruation (into fallopian tube)
  • metaplasia
  • vascular/lymphatic dissemination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Obstetric Conditions (3)

A
  • Spontaneous Abortion
  • Ectopic Pregnancy
  • Toxemia of Pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Spontaneous Abortion

A
  • miscarriage
  • occurs in 10-15% of recognized pregnancies and 50% of all pregnancies
  • most in first trimester are b/c of chromosomal abnormality
  • later loss more commonly include hormonal insufficiency, infection, inflammation, trauma
  • most of the time the miscarriage is not investigated unless a malformed fetus or 3+ spontaneous abortions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Ectopic Pregnancy

A
  • implantation of the fetus somewhere other than the uterus
  • 90% in fallopian tubes
  • 1/150 pregnancies
  • tubal obstruction: 1/3-1/2 patients have PID
  • classic presentation of severe abdominal pain 8-10 weeks after last menstrual period
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Toxemia of Pregnancy

A
  • pre-eclampsia/eclampsia
  • need hypertension, proteinuria, AND edema
  • about 6% of all pregnant women
  • usually in 3rd trimester
  • some develop seizures and DIC (eclampsia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Toxemia of Pregnancy: Treatments (4)

A
  • bed rest
  • dietary
  • BP drugs
  • delivery of infant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Common Gynecological Neoplastic Conditions (5)

A
  • Vulvar and Vaginal Carcinoma
  • Uterine Carcinoma
  • Endometrial Carcinoma
  • Myometrium
  • Ovary and Uterine Tube tumors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Vulvar and Vaginal Carcinoma

A
  • most squamous cell
  • HPV related (younger women) or Non-HPV related (older women)
  • Treatment is surgical, radiation & chemotherapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Uterine Cervical Carcinoma

A
  • common worldwide
  • PAP smear screenings v effective at preventing invasive carcinoma
  • mostly squamous cell carcinoma
  • mortality usually associated from invasion, not metastasis
  • HIGHLY associated with HPV (>95%)
  • strains 16&18 highest risk, but most cases of HPV do not result in cervical cancer
  • HPV vaccine at 11-26 yrs
  • Treatment: surgical, radiation, chemo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Types of Surgery for Uterine Cervical Carcinoma

A
  • Radical Hysterectomy: higher stage, removes uterus and upper vagina
  • Radical Trachelectomy: removal of cervix but leave body of uterus intact (preserves fertility)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Endometrial Carcinoma

A
  • “type I”: 55-65 yrs, present with post-menopausal uterine bleeding
  • risk factors: age, obesity, diabetes, hypertension, infertility, unopposed estrogen
  • often cured by hysterectomy
  • subgroup of patients more aggressive (looks like ovarian cancer)
  • treatment: surgical, radiation, chemotherapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Myometrium (2 types)

A
  • leiomyoma (fibroid)
  • benign, common
  • symptoms include abnormal bleeding, compression of bladder, infertility, pain
  • leiomyosarcoma
  • malignant, rare
  • does not arise from pre-existing leiomyoma
  • treatment mainly surgical
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Ovary and Uterine tube tumors

A
  • most ovarian tumors in premenopausal women are benign

- most ovarian tumors in postmenopausal women are malignant

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

Ovary and Uterine tube tumors: cells of origin

A
  • epithelial tumors
  • germ cell tumors
  • sex cord-stromal tumors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Ovary and Uterine tube tumors: Benign Tumors

A
  • 80%
  • mature teratoma (dermoid cyst)
  • very commonly hair and skin formation
  • benign cystademona: of epithelial origin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Ovary and Uterine tube tumors: Malignant Tumors

A
  • most are epithelial tumors
  • serous carcinoma
  • mucinous carcinoma
  • endometriod carcinoma
  • poor prognosis
  • treatment: aggressive surgery, chemo, radiation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Non-Neoplastic Conditions of Male Repro (8)

A
  • STIs
  • Hypospadias
  • Cryporchidism
  • Testicular Torsion
  • Epididymitis
  • Granulomatous orchitis
  • Prostatitis
  • Benign prostatic hyperplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Hypospadias and epispadias

A
  • congenital maldevelopment of the urethral groove that results in the urethral opening on either the ventral or dorsal aspect of the penis
  • hypospadias is more common (1 in 300)
  • complications: higher chance of urinary tract obstruction and infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Cryptorchidism

A
  • undescended testes
  • 25% of cases of cryptochidism are bilateral
  • arrested sperm development and scaring, infertility
  • 5-10x increase risk of developing testicular cancer
  • most descend on own by age 1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Surgery to place testis into scrotal sac

A
  • orchiopexy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Testicular Torsion

A
  • twisting of the testis which obstructs venous flow
  • bell clapper deformity (fusion of scrotum and things that tether testis)
  • occurs around puberty
  • severe pain
  • surgical de-torsion performed w/ fixation of the testis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

De-torsion at 4-6 hrs vs 12 hours vs 24 hours viability

A
  • 4-6: 100% viability
  • 12: 20% of testes are still viable
  • 24: no viability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Epididymitis

A
  • inflammation of the epididymis as a result of infections that travel from the urinary tract down to the epididymis
  • chlamydia most common cause in young adult men
  • UTI most common cause in older adult men
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Granulomatous orchitis

A
  • granulomous inflammation of the testis
  • rare
  • can occur from tb or leprosy
  • mostly idiopathic cause
  • present clinically with tender testicular mass and fever or painless, enlarged testis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Prostatitis (3 types)

A
  • Acute Prostatitis
  • Chronic Prostatitis
  • Granulomatous Prostatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Acute Prostatitis

A
  • result of UTIs or after catheterization

- present with fever, dysuria, and very tender prostate

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

Chronic Prostatitis

A
  • may be from bacterial infection or not.
  • presents with low back pain, dysuria, pubic and perineal pain
  • usually independent of acute prostatitis
  • treatment difficult
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Why is treatment of chronic prostatitis difficult?

A
  • most antibiotics penetrate the prostate poorly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Granulomatous prostatitis

A
  • can be due to infectious agents (e.g. tb and fungi)
  • also could be secondary to BGG
  • possible to be non-specific also, from a rxn to ruptured ducts in the prostate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Benign Prostatic Hyperplasia (BPH)

A
  • nodular hyperplasia
  • increase in prostatic tissue
  • can be considered normal b/c it occurs so often as one ages
  • 20% of 40 yr old men, 90% of 80 yr old men
  • clinical symptoms: nocturia, difficulty urinating, initiating and stopping urination, dysuria, UTI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What causes growth of the prostate? (2 hormones)

A
  • testosterone
  • dihydroxytestosterone
  • more potent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Therapy for BHP

A
  • 5-a reductase inhibitors
  • a1- adrenergic receptor blockers
  • transurethral resection of prostate (TURP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Neoplastic Male Repro Conditions (3)

A
  • Penile Cancer
  • Testicular Cancer (germ cell tumors and lymphoma)
  • Prostate Carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Penile Cancer

A
  • carcinoma in-situ (no access to lymphatic channels) and invasive carcinoma
  • less than 1% of male cancers in US
  • associated with HPV, smoking, poor hygiene
  • circumcision reduces risk, but US risk is also very low
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Testicular Cancer: Germ Cell Tumors

A
  • peak incidence 15-34 yrs of age
  • two subtypes:
  • seminoma (most common), good prognosis, usually caught early
  • non-seminoma: higher stage of diagnosis, worse prognosis
    • one type is teratoma (usually malignant)
  • risk factors: Race (white more common), Family History
  • Often secrete hormones or enzymes
  • common sites of metatstasis: retroperitoneal lymph nodes, other lymph nodes, lungs, liver, brain bones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Spermatocytic seminoma

A
  • much older average age (>65) and very good prognosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Testicular Cancer: Lymphoma

A
  • systemic malignancy (present in many areas of body)

- most common cancer in the testes in men over 60

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

Prostate Carcinoma: Clinical Presentation

A
  • Nodule on rectal exam
  • elevated PSA
  • occasionally urinary symptoms
  • symptoms from metastasis (bone pain)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Prostate Carcinoma: Etiology (Risk Factors) (5)

A
  • Age: risk increases with age
  • Race: common in blacks and whites, not asians
  • Diet: dietary fat increase risk, lycopenes decrease risk
  • Androgens
  • Genetics: 8-10%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Prostate Carcinoma: Prognostic Factors

A
  • Stage: most important

- Grade: relatively more important in prostate cancer than some other cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Prostate Carcinoma: common sites of metastasis

A
  • bone (most common)
  • lung
  • liver
  • brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Prostate Carcinoma: Treatments

A
  • wait
  • surgery
  • radiation
  • hormonal therapy (anti-androgens)
  • chemo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Eunuch

A
  • castrated male

- will not get benign prostatic hypertrophy nor prostate cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Acute Kidney Injury refers to

A
  • process that happens within hours to days that prevents clearance of waste products from the blood
  • is potentially reversible
  • increase in serum creatinine or reduction in urine output
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

azotemia

A
  • buildup of nitrogenous waste products in the blood
  • detected by blood urea nitrogen (BUN) levels
  • preferred lab measurement is the serum creatinine test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

urine output of

A
  • oliguric
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

urine output of

A
  • anuric
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Uremia

A
  • clinical syndrome of organ dysfunction that results from azotemia
  • presents with fatigue, nausea, neuropathy, paricarditis, asterixis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

asterixis

A
  • flapping of the hands

- symptom of uremia AKI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Serum Creatinine Test

A
  • AKI measurement

- creatinine is produced by all muscles and should be filtered by the kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Etiology (Causes) of AKI

A
  • pre-renal (low blood flow to kidney)
  • post-renal (blockage so urine cannot flow)
  • problem with glomeruli, tubules, or interstitum (intra-renal)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Pre-Renal AKI

A
  • major issue is lack of blood flow from various insults

- fixed by fixing insult (i.e. septic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Post-Renal AKI

A
  • not common
  • usually “plumbing issue”, something is blocking exit
  • ex.) elderly man with enlarged prostate blocks the free flow of urine
  • need renal ultrasound to see if hydronephrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

hydronephrosis

A
  • ureters and renal pelvis distended secondary to blockage of urine
  • related to Post-Renal AKI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Intrinsic AKI (3) (what can be found in the urine?)

A
  • casts (tubular proteins that trap RBC, WBC) commonly found in the urine
  • Acute Interstitial Nephritis (AIN)
  • Glomerulonephritis (GN)
  • Acute tubular necrosis (ATN)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Acute Interstitial Nephritis

A
  • AIN
  • inflammation of the interstitium
  • usually from medications that elicit a hypersensitivity rxn
  • urine has WBCs
  • mononuclear cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Glomerulonephritis

A
  • GN
  • inflammation of the glomeruli
  • presence of blood and protein in the urine
  • can be immune-complex mediated (Wegener’s granulomatosis) or non-immune complex mediated (post-streptococcal GN, traveled to kidneys)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Acute Tubular Necrosis

A
  • ATN
  • supply of oxygen and nutrients to the kidney tubules is insufficient to meet their metabolic demands
  • can also occur when tubule cells exposed to a toxic agent
  • extreme ATN has a loss of many tubules simultaneously, little or no urine output
  • if tubular basement membrane remains intact, can heal itself over time.. if fibrosis, permanent damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Two types of renal replacement therapy (dialysis)

A
  • hemodialysis

- peritoneal dialysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Hemodialysis

A
  • blood and clean fluid run countercurrent to each other through an artificial filter
  • 3x/week, in a clinic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Peritoneal dialysis

A
  • uses the peritoneum as a filter
  • dialysate is placed directly into the abdominal cavity and overtime toxins diffuse from the capillaries into the abdominal cavity
  • done daily, at home
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

why is an AKI transplant unique?

A
  • do not remove ‘old’ kidney, just place new one beside it
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Chronic Kidney Disease (CKD)

A
  • kidney damage present for >3 months
  • and that damage most commonly confirmed with a loss of GFR
  • 5 stages (1 is essentially normal GFR and stage 5 needs RRT)
  • irreversible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Pathology of CKD

A
  • destruction of either glomeruli or renal tubules leads to functional loss of the nephron
  • each remaining nephron takes on an additional workload (single-nephron GFR) but that causes them to become injured faster (super-nephron hypothesis)
  • adaption can take place until less than 20% of the normal nephrons are left
  • eventually, nonfunctioning nephrons are replaced by fibrosis tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Uremic Syndrome

A
  • clinical syndrome of azotemia associated with organ dysfunction
  • when the kidneys are no longer able to maintain a balance b/c the workload is too large
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Typical Symptoms are Uremia

A
  • fatigue
  • increased irritability
  • difficulty breathing
  • nausea
  • itching
  • edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Typical signs/altered lab values of uremia

A
  • hypertension
  • edema
  • anemia
  • acidosis
  • low serum calcium
  • high serum phosphate and/or potassium
  • high levels of nitrogenous waste
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Medications to help protect the kidneys over time

A
  • ACE inhibitors (prevent angiotension 1 to angiotensin 2)
  • keeps BP and aldosterone down to lessen salt retension
  • Angiotension receptor blockers (ARBs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Estimating GFR (general)

A
  • inputs for creatinine level, age, if female, if african american
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Most common causes of CKD in the US (4)

A
  • diabetes, hypertension, glomerular disease, polycystic kidney disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Patients with CKD are at high risk for what other disease?

A
  • cardiovascular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Stages of CKD are determined by what two broad factors?

A
  • Hypertension/Lab abnormalities

- Clinical Symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Risk factors for progression of CKD

A
  • Hypertension
  • Proteinuria
  • Diabetes
  • Smoking
  • Hyperlipidemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Who are kidney transplants usually given to?

A

stage 4 or 5 CKD, rare to get transplant if AKI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

US stats on STIs

A
  • 20 mil new STI cases/yr

- 50% in 15-24 yr olds (reporting bias in minorities)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Types of Bacterial STIs (4) in order of prevalence

A
  • Chlamydia
  • Gonorrhea
  • Syphilis
  • Chancroid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Treponema Pallidum

A
  • Syphilis, leus
  • spirochete organism
  • causes systemic disease in multiple forms
118
Q

Treponema Pallidum: Clinical Features primary stage

A
  • chancre 3 weeks after infection
119
Q

Treponema Pallidum: Clinical Features secondary stage

A
  • 2-10 weeks after chancre
  • rash on palms and soles
  • condyloma lata (lesions in genital area)
  • lesions contain organisms
  • sometimes fever, headache, arthritis
120
Q

Treponema Pallidum: Clinical Features tertiary stage

A
  • rare to develop in US
  • inflammatory lesions, low amts of organism
  • spread to aorta, CNS, gummas in skin, bones
  • occurs years after primary infection
121
Q

gumma

A
  • tertiary stage of syphilis

- granuloma like lesions

122
Q

Congenital Sphyilis

A
  • greatest risk when mother is in primary or secondary stage
  • or late in pregnancy b/c easier to cross placenta s
  • stillbirth in ~20-40% of untreated cases
123
Q

syphilis pathogenesis

A
  • chronic inflammation and scarring involving blood vessels
124
Q

syphilis diagnosis & treatment

A
  • cannot be cured
  • use treponemal test against antibody (specific)
  • non-treponemal test: (non specific) reflects disease activity
  • treatment: penicillin
125
Q

Neisseria Gonorrhoaea

A
  • gonorrhea

- facultative intracellular (can live in and outside cell)

126
Q

Neisseria Gonorrhoaea: clinical features

A
  • urethritis
  • epididymitis
  • PID
  • endometrium usually spared from infection
  • Pharyngitis
  • proctitis (inflammation of rectum and anus)
  • common to have co-infection w/ chlamydia
127
Q

Neisseria Gonorrhoaea passed from mother to baby

A
  • can cause blindness
  • joint infection
  • sepsis
128
Q

Neisseria Gonorrhoaea Diagnosis

A
  • gram stain of discharge
  • culture
  • DNA probe (most common)
129
Q

Neisseria Gonorrhoaea Treatment

A
  • generally treated for both gonorrhea and chlamydia at the same time (sometimes before test results back)
  • antibiotic resistance is becoming a problem
130
Q

Chlamydia trachomatis

A
  • serotypes D-K commonly seen in the US
131
Q

Chlamydia trachomatis: clinical features

A
  • infects similar sites to gonorrhea
  • often mild symptoms or asymptomatic but still does chronic damage (PID, infertility)
  • associated with preterm delivery
132
Q

Chlamydia trachomatis: Diagnosis

A
  • DNA probe most commonly used
133
Q

Chlamydia trachomatis: Treatment

A
  • azithromycin, doxycycline

- usually treated for gonorrhea as well b/c commonly co-infect

134
Q

Haemophilis ducreyi

A
  • chancroid
  • gram negative coccobacillus
  • common in the tropics
  • associated with uncircumcised men and poor personal hygiene
  • sores appear 4-7 days after exposure and open up to lesions
  • associated with HIV spread
135
Q

Haemophilis ducreyi diagnosis & treament

A
  • culture or PCR

- treatment: azithromycin, ceftriaxone, erthyromycin, ciprofloxacin

136
Q

Viral STIs (3)

A
  • HPV
  • HSV (herpes simpex)
  • HIV
137
Q

HPV (capsulated/non-capsulated)(what type of cell it infects) (two general types)

A
  • NON-ENCAPSULATED DNA virus
  • infects basal epithelium of squamous mucosa
  • 100+ types identified
  • clinical features:
  • asymptomatic
  • low risk (6,11) genital warts
  • high risk (16&18) may lead to dysplasia and carcinoma
138
Q

Herpes Simplex Virus

A
  • HSV
  • ENCAPSULATED DNA virus
  • two types: HSV-1 (infects mouth) & HSV-2 (infects genitals)
139
Q

HSV clinical features

A
  • infects epithelium of skin and mucous membranes
  • enters the sensory neurons around the site of infection
  • symptoms only occur in 1/3 infected
  • blistering lesions that heal in 1-4 wks
  • increased susceptibility to HIV
  • subsequent outbreaks not a severe as the first
140
Q

HSV and transmission

A
  • can occur in both active and latent phases, but more likely in the active phase
141
Q

HSV and pregnancy/birth

A
  • can be passed from mom to baby in birth canal

- may be fatal to the infant

142
Q

HSV diagnosis & treatment

A
  • serology: sensitive and specific

- no cure; some antiviral agents prevent outbreaks and shorten duration/severity

143
Q

HIV

A
  • ENCAPSULATED RNA virus
  • replicates by reverse transcription (retrovirus)
  • infects cells that express CD4 on surface (T-cells)
144
Q

Transmission of HIV

A
  • via exchange of bodily fluids
  • sexual
  • parenteral inoculation (needle sharing)
  • mother to infant (birth canal, breast milk, transplacental)
  • NOT through casual contact
145
Q

At risk groups in US adult population for HIV

A
  • Homosexual & bisexual men
  • intravenous drug abusers
  • hemophiliacs or other who received blood or organs (before 1985)
  • heteros who have had contact with any above group
146
Q

HIV clinical course (3 stages)

A
  • acute retroviral syndrome (flu-like)
  • chronic asymptomatic phase (7-10 yrs)
  • continuous HIV production, steady decline in CD4 T-Cells
  • AIDS
  • fever, fatigue, weight loss, severe opportunistic infections & neoplasms, neurological diseases
147
Q

HIV diagnosis

A
  • test for antibodies to HIV

- test for viral nucleic acids in blood by PCR

148
Q

HIV treatment

A
  • Highly Active Antiretroviral Therapy (HAART)
149
Q

Protozoal STI

A
  • Trichomas Vaginalis
  • adheres to mucosal surface, does not invade
  • motile
150
Q

Trichomas Vaginalis: Clinical Features

A
  • asymptomatic
  • itching
  • discharge (vaginal or penile) fishy odor, yellow-green
  • urinary frequency and/or dysuria
  • dyspareunia (painful intercourse)
151
Q

Trichomas Vaginalis: Diagnosis and Treatment

A
  • small red ulcerations present on vaginal wall or cervix

- treatment: metronidazole, tinadazole

152
Q

General functions of the skin

A
  • physical barrier
  • immune organ
  • provide pigment
  • produce vitamin D
  • absorptive ability
153
Q

basal cells of skin

A
  • like the “stem cells” of the skin
154
Q

What cells produce melanin

A
  • melanocytes

- malignant melanoma from melanocytes

155
Q

two most common neoplasms of the epidermis

A
  • squamous cell carcinoma
  • basal cell carcinoma
  • both more common in older populations
  • rarely lethal
  • most common types of cancer in the US but easily treated so they are not included in statistics
156
Q

Melanoma

A
  • malignant neoplasm from melanocytes
  • related to sun exposure
  • arises in a younger population, spreads widely throughout the body
  • affects unusual sites like acral skin, eyes, nail beds, internal organs
  • incidence rising due to UV exposure from sunlight
157
Q

Melanoma clinical manifestation

A
  • naked eye best way to detect

- use ABCDE criteria

158
Q

Nevus

A
  • mole, collection of cells present in an unusual location or excessive number
159
Q

ABCDE criteria for melanoma identification

A
  • A: asymmetry (two halves are not mirror images
  • B: border irregularity (outlines are not rounded and smooth)
  • C: color (not uniformly colored)
  • D: diameter >6mm
  • E: Evolution (does it change overtime)
160
Q

Pathogenesis of Melanoma

A
  • UV radiation in sunlight makes DNA damage
  • formation of pyrimidine dimers
  • accumulation of ROS
  • melanin usually an antioxidant
  • mutations in pro-growth factors, & telomerase
161
Q

Diagnosis of Melanoma

A
  • excision and examination of the specimen
  • two most important prognosis factors are thickness and ulceration
  • thin ones can be removed and person cured immediately
162
Q

Melanoma next two most important prognosis factors

A
  • lymph node metastasis and distant metastasis
163
Q

what is rare about distant metastasis in melanoma?

A
  • affects organs not usually involved (spleen and heart)
164
Q

Acne Vulgaris

A
  • caused by infection of plugged sebaceous glands

- refined categorization by age group, etiologic agent, distribution, or severity

165
Q

What plugs sebaceous glands?

- what is it called when bacteria infect the plug

A
  • mixture of keratin and sebum (oily product of gland)

- when bacteria colonize the plug it forms a comedone

166
Q

comedone below skin surface vs above

A
  • below: whitehead

- above: blackhead

167
Q

What happens when sebaceous plug ruptures?

A
  • releases pro-inflammatory factors
  • WBC clean up debris and pustule forms
  • fusion of pustules can lead to nodule and cyst formation
168
Q

what is the most severe form of acne?

A
  • nodule and cyst formation
169
Q

Risk factors for acne vulgaris

A
  • androgen production (male, puberty, steroids, stopping birth control pills, pregnancy..)
  • stress (increases androgen production
  • family history
  • skin irritation
  • some medications
170
Q

Treatment for acne

A
  • aimed at restructuring the follicles and eliminating the bacterial superinfection
  • use retinoids to normalize epithelial cell maturation
  • topical (benzoyl peroxide) and oral antibiotics most commonly used
171
Q

Cellulitis

A
  • infection of the skin caused by staphylococcal or streptoccocal bacteria
  • can result in skin necrosis if not treated, bacteremia, and septic shock
172
Q

Dermatitis

A
  • inflammation of the skin; a reaction pattern
  • red, itchy rash
  • variety of causes such as autoimmune, hypersensitivity, genetic, toxins etc
  • variety of environmental triggers: sunlight, drugs, chemicals, temperature, stress
  • usually not infectious
173
Q

Contact Dermatitis

A
  • localized skin rxn to an irritant only @ site of contact with the skin
  • two types:
  • irritant contact derm
  • allergic contact derm (auto-immune)
174
Q

Irritant contact derm

A
  • general improvement with time
  • resolves relatively quickly after cessation of exposure
  • ex. rubbing alcohol, cosmetic products, sawdust
175
Q

Allergic Contact Derm

A
  • initial exposure sensitizes T-cells to an antigen
  • subsequent exposure elicits a T-cell mediated localized immune rxn
  • common offenders: poison ivy, nickel, latex, UV light (photo-allergic contact dermatitis)
176
Q

Treatments of Dermatitis

A
  • avoid contact with irritant
  • prescription steroid creams
  • antihistamines for itching
177
Q

Complications to Dermatitis

A
  • secondary skin infection

- chronic, itchy, scaly skin due to chronic itching

178
Q

Atopic Dermatitis

A
  • ex. eczema

- patches of dry, itchy skin in a person with allergies, asthma, or hay fever

179
Q

Seborrheic Dermatitis

A
  • dandruff, cradle cap

- red rash associated with waxy scaly plaques on scalp

180
Q

Interstitial Lung Diseases

A
  • characterized by lung injury
  • pulmonary inflammation related to known or unknown causes
  • variable degrees of fibrosis
181
Q

Types of Interstitial Lung Disease (4)

A
  • Idiopathic Pulmonary Fibrosis (IPF)
  • Sarcoidosis
  • Hypersensitivity Pneumonitis
  • Pneumoconiosis
182
Q

Idiopathic Pulmonary Fibrosis

A
  • fibrotic interstitial lung disease
  • unknown etiology
  • seen as an end result to other lung diseases
  • presents as progressive dyspnea and dry cough
  • diagnosed by chest CT
  • typically seen in males >55
  • 50% of patients die within 5 years
  • no effective treatments
  • lung transplantation is the only cure
183
Q

Lung Transplantation

A
  • only for terminal lung diseases (COPD, cystic fibrosis, IPF)
  • single lung (IPF, COPD) or double lung (CF)
  • high risk surgery
  • average survival after transplantation is only 5 yrs
  • other limitations such as high cost, availability
184
Q

Pathogenesis of IPF (two “stages”)

A

Usual Interstitial Pneumonia (UIP)
- alveolar walls thickened with extensive fibrosis
- extreme abnormalities in alveolar architecture
Desquamative Interstitial Pneumonia (DIP)
- milder/earlier type of this disease
- minimal fibrosis, alveolar inflammation, and fulness of alveoli with macrophages

185
Q

Two new drugs for IPF (general info)

A
  • nintedonib and pirfendone
  • slow down progression but do not cure
  • $$$$$
186
Q

What to do to “help” IPF?

A
  • vaccinations for flu and pneumonia
  • pulmonary rehab and oxygen therapy
  • palliative care (live longer this way than with aggressive treatments)
  • corticosteroids if they help
187
Q

Sarcoidosis

A
  • chronic granulomatous interstitial lung disease of idiopathic origin
  • lungs most affected but can also be in eyes, skin, liver, spleen, bones, muscles, lymph nodes etc
  • patients often present with dyspnea and cough
  • most patients it resolves itself spontaneously
  • in cases where it is not spontaneously resolved, treatment with corticosteroids
  • the more severe it comes in, the more likely it will resolve itself
188
Q

Pathogenesis of Sarcoidosis

A
  • activation of T-Lymphocytes
  • formation of granulomas
  • minimal fibrosis
189
Q

Stages of Sarcoidosis

A
  • stage I: lymph nodes (“Idaho Potato”)
  • stage 2: lymph nodes and parenchyma
  • stage 3: parenchyma disease
190
Q

Ethnic Vulnerability of Sarcoidosis

A
  • AA Women + +
  • N Europeans +
  • Asians - -
191
Q

Hypersensitivity Pneumonitis

A
  • Exterinsic Allergic Alveolitis
  • pulmonary inflammation secondary to immune rxn to inhaled ORGANIC dusts
  • most common are found in moldy hay (farmer’s lung disease) and bird droppings (bird feeder’s disease)
  • two main syndromes
  • acute: manifests rapidly after exposure to a fever, cough and dyspnea within a few hours of exposure and resolves in 24 to 48 hours
  • chronic: low grade exposure over a long period of time, hard to connect to disease. cough and progressive dyspnea
  • main treatment is avoidance of exposure to the offending agent and corticosteroids
192
Q

Pneumoconioses: what it is and the two types

A
  • caused by inhalation of INORGANIC dusts
  • cause pulmonary inflammation associated with granulomas and a varying degree of fibrosis
  • Silicosis
  • Asbestosis
193
Q

Silicosis

A
  • caused by inhalation of silicon dioxide (silica)
  • occurs in mining, sandblasting, and foundries
  • causes pulmonary inflammation and fibrosis
  • symptoms generally minimal in cases of simple silicosis
  • x-ray findings and history sufficient for diagnosis
  • do not require treatment generally, but at increased risk for developing TB
194
Q

Asbestosis

A
  • fibrotic pulmonary disease caused by inhalation of asbestos
  • occurs in mining, insulation, tile production, and ship building
  • inhaled asbestos fibers deposit in distal airways and alveoli and are ingested by macrophages
  • asbestos bodies form (asbestos fibers surrounding with iron rich protein)
  • clinically apparent 20-30 years post exposure
  • progressive dyspnea and cough
195
Q

Other conditions resulting from asbestosis

A
  • pleural plaques
  • pleural effusion
  • mesothelioma
  • increased risk for bronchogenic carcinoma esp in smokers
196
Q

Mesothelioma

A
  • can result from asbestosis
  • cancer of the pleural surface
  • need very low level to trigger
  • very lethal cancer
197
Q

What level risk from combination of asbestos exposure and smoking to get bronchogenic carcinoma

A
  • 100 fold increase
198
Q

Lung Cancer

A
  • 1/4 of all cancer deaths
  • more people die from lung cancer than from breast, colon, and prostate cancers combined)
  • carcinoma of the lung is the most common cause of death of men and women in the US (160,000 deaths/yr)
  • 225,000 new cases/yr
  • most types present with persistent cough, sputum, weight loss, and hemoptysis
  • diagnosis by chest x-ray and tissue examination
199
Q

Small Cell carcinoma

A
  • highly malignant cancer
  • poor prognosis because usually caught late
  • majority of patients have metastasized before diagnosis
  • unpredictable
200
Q

Non-small cell carcinoma

A
  • more localized and metastasize slower

- includes large cell carcinoma, squamous cell carcinoma, and adenocarcinoma

201
Q

Treatment of Lung Cancers

A
  • main therapy for small cell: chemo
  • main therapy for non-small cell: surgery
  • molecular marker targeted therapy now starting to be used
202
Q

Pyelonephritis

A
  • inflammation of the kidney
  • usually due to bacterial infection
  • viruses and fungi possible, but unlikely (mainly in immunocompromised patients)
203
Q

Route of infection of Pyelonephritis

A
  • Hematogenous

- Ascending

204
Q

Hematogenous Route of Pyelonephritis

A
  • via the bloodstream
  • less common
  • usually occurs when sepsis or endocarditis
  • more likely to be viruses and fungi if this way
205
Q

Ascending Route of Pyelonephritis

A
  • via lower urinary tract (urethra and bladder)

- most common route of infection

206
Q

Clinical presentation of acute pyelonephritis

A
  • fever
  • costovertebral angle tenderness (back where kidneys are is very tender)
  • bladder/urethral symptoms (dysuria. frequency, urgency)
207
Q

Risk factors for pyelonephritis (8)

A
  • Gender and Age
  • Partial Anatomical obstruction of urinary tract
  • neurogenic bladder
  • instrumentation of bladder (catheter)
  • pregnancy
  • diabetes
  • immunosuppression
  • vesicoureteral reflux
208
Q

Pyelonephritis Gender and Age risk factor

A
  • overall more women than men

- very young and over age 40, more men than women

209
Q

Neurogenic Bladder

A
  • improper filling and emptying of bladder due to abnormality of its nerve function
210
Q

Diabetes in Pyelonephritis

A
  • immunosuppressed
  • bacteria adhere more easily to their walls
  • may develop neurogenic bladder
  • glucosuria provides substrate for bacteria to grow
211
Q

Vesicourteral Reflux

A
  • urine flowing retrograde up the ureter due to “one way valve” not proper
212
Q

Organisms associated with Pyelonephritis

A
  • Escherichia Coli (85% of infections)

- other organisms usually found in GI tract or skin organisms

213
Q

Bacterial Virulence Factors with pyelonephritis

A
  • fimbriae: filamentous proteins on surface of bacteria that allow the bacteria to adhere easier
  • P fimbrae are expressed in some E. coli strains and are able to bind to galactose-galactose molecules on surface of epithelial cells lining the urinary tract
214
Q

Pathologic findings of pyelonephritis: urinalysis

A
  • cloudy urine b/c of pyuria, hematuria, proteinuria, and high pH
  • find leukocyte casts as well (cylindrical shape)
215
Q

pyuria

A
  • WBC in urine
216
Q

Acute pyelonephritis pathologic findings

A
  • rarely seen b/c usually treated right away
  • neutrophilic inflammation of renal tubules and interstitum
  • rare cases form abscess (more severe)
217
Q

Chronic pyelonephritis pathologic findings

A
  • small, shrunken kidneys
  • scarring on surface of kidney to calyx
  • tubular dilation and chronic inflammation
218
Q

Cystic Kidney Diseases (5)

A
  • Simple Cyst
  • Autosomal Dominant Polycystic Kidney Disease
  • Autosomal Recessive Polycystic Kidney Disease
  • Renal Cystic Dysplasia
  • Acquired Renal Cystic Disease
219
Q

Simple Cyst

A
  • very common and may occur at any age
  • usually one, maybe more thin-walled cysts on surface of kidney filled with clear or yellow fluid
  • usually asymptomatic w/ no complications
  • may rupture if too large
220
Q

Autosomal Dominant Polycystic Kidney Disease

A
  • AKA Adult Polycystic Kidney Disease
  • fairly common
  • always BILATERAL
  • loss of renal function in 30s or 40s
  • may have hematuria
  • may have pain due to pressure from enlarged kidney or due to passage of blood clots
  • both kidneys MASSIVELY ENLARGED
  • hundreds of cysts
  • about 10% of all renal failure patients are from APKD
  • associated with intracranial aneurysms and mitral valve prolapse, asymptomatic cysts in other organs (liver)
221
Q

Genes associated with Autosomal Dominant Polycystic Kidney Disease

A
  • PKD1 and PKD2
  • PKD1 = 85% of cases
  • thought to play a role in adhesion between cells and adhesion of cells to surrounding matrix
  • results in overactive proliferation of tube cells, overactive secretion of fluid, and fibrosis
222
Q

Autosomal Recessive Polycystic Kidney Disease

A
  • AKA childhood Polycystic Kidney Disease
  • rare
  • always BILATERAL
  • renal failure in infancy/childhood
  • enlarged kidneys with SMOOTH surface
  • hundreds elongated cysts that run perpendicular to surface of the kidney
  • mutations of the PKHD1 which encodes fibrocystin
  • usually liver has cysts as well
  • if child lives long enough, may develop liver fibrosis and failure (congenital hepatic fibrosis)
  • best chance for survival is both a kidney and liver transplant
223
Q

What is unique about transplants with Adult and Childhood Polycystic Kidney Disease?

A
  • take the old kidneys out

- too large for body

224
Q

Renal Cystic Dysplasia

A
  • Multicystic Dysplastic Kidney
  • Dysplastic refers to abnormal development, not cancer
  • may be unilateral or bilateral
  • if unilateral –> flank mass in young child
  • if bilateral –> may present with kidney failure in newborn
  • slightly enlarged and irregular
  • 20-50 cysts
  • Islands of abnormal structures (cartilage, undifferentiated mesenchyme, immature collecting ducts)
  • pathogenesis is abnormal metanephric differentiation
  • outcome depends on whether it is unilateral or bilateral
225
Q

Acquired Renal Cystic Disease

A
  • affects men more than women
  • occurs from long term dialysis treatment
  • small “end-stage” kidneys
  • multiple cysts inside
  • complications: hematuria, renal cell carcinoma may develop
  • non-functioning kidney anyways
226
Q

Regulation of PaCO2

A
  • 1:1 relationship between CO2 production and ventilation
  • hyperventilation: reduced PaCO2
  • hypoventilation: increased PaCO
227
Q

Alveolar Hyperventilation associated disease states

A
  • low PaCO2
  • Fever, sepsis
  • medications
  • metabolic acidosis
  • maximum exercise
  • hypoxemia
  • anxiety
228
Q

Alveolar Hypoventilation assocated disease states

A
  • CNS depression
  • Airway Obstruction
  • Chest wall restriction
  • Advanced interstitial lung disease
  • neuromuscular disorder
229
Q

hypoxemia

A
  • reduction of PaO2
230
Q

5 mechanisms of hypoxemia

A
  • Low inspired oxygen: airplanes, high altitude
  • Impaired diffusion (thick membranes)
  • Hypoventilation
  • Low V/Q; ventilation/perfusion ratio low
  • Right-to-left shunt
231
Q

Right-to-left shunt: hypoxemia

A
  • venous blood reaches systemic circulation w/o contacting alveolar oxygen
232
Q

Residual Volume

A
  • volume of air remaining at the end of forced exhalation
233
Q

Functional Residual Capacity

A
  • volume of gas remaining in lung after normal exhalation
234
Q

Inspiratory Capacity

A
  • volume inspired rom normal-end exhalation

- dependent on inspiratory muscle strength

235
Q

Vital Capacity

A
  • volume of air inhaled or exhaled between maximum inspiratory and expiratory effect
236
Q

Resistance vs Elastance

A
  • Resistance: how difficult airflow is through airways

- Elastance: how well the lung and thorax stretch

237
Q

Elastic properties plotted on graph (axes)

A
  • volume vs pressure
  • highest TLC is emphysema (hyperinflation)
  • lowest TLC is fibrosis (restriction)
238
Q

Restrictive Lung Disease hallmark

A
  • Reduced TLC
239
Q

Two categories of restrictive lung disease

A
  • restriction secondary to parenchymal abnormality (e.g. fibrosis)
  • TLC reduced with rest of lung volumes
  • restriction secondary to respiratory muscle weakness (eg. ALS)
  • TLC is reduced along with IC (too weak to take a deep breath)
  • RV is increased b/c patient is too weak to exhale maximally
240
Q

Pathophys of Airflow obstruction (hallmark)

A
  • FEV1/FVC reduced
241
Q

Mechanisms of Airflow Obstruction (2)

A
  • narrowing of airway lumen (increased thickness of airway wall & mucus and secretions that block airway)
  • Dynamic airway narrowing (destruction of elastin fibers that decrease support and are prone to collapse when pressure in chest increases b/c of inhalation)
242
Q

Spirometry

A
  • tests lung forced vital capacity
  • how much air in lung (-RV)
  • test FEV1: how much air out in first second compared to total
  • normal is 75-85% total capacity in first second
243
Q

Pulmonary Hypertension

A
  • increased pressure in the pulmonary vascular system
244
Q

Two main patterns of Pulmonary Hypertension

A
  • Acute (pulmonary embolism) and Chronic (result of chronic lung disease, recurrent thromboembolisms, congenital heart disease, and left heart failure
245
Q

Primary Pulmonary Hypertension

A
  • extreme fibrosis and very little blood flow
  • leads to rapid death in most patients
  • idiopathic cause
246
Q

Pulmonary Embolism

A
  • lodging of a preformed clot in pulmonary vasculature
  • raises pulmonary pressure
  • most clots originate in deep veins of legs and break off and travel to lungs
  • symptoms: shortness of breath & chest pain, increased respiration, pulse rate, low PaO2 and PaCO2
  • MOST clots fragment and lyse in a few days
247
Q

Adult Respiratory Distress Syndrome (ARDS)

A
  • clinical syndrome of rapidly progressing respiratory failure characterized by severe hypoxemia
  • typically seen in previously healthy patient who sustained a severe injury or other catastrophic illness
  • results from diffuse alveolar damage (DAD): non-specific pattern of pulmonary parenchymal reaction
248
Q

Potential causes of ARDS

A
  • Severe infection
  • multiple trauma
  • aspiration
  • pancreatitis
  • shock
249
Q

Pathogenesis of ARDS

A
  • main mechanism for DAD is sever lung injury resulting in endothelial and epithelial damage
  • results in leakage of protein-rich fluid from capillaries into alveolar space and loss of type-1 pneumocytes
  • inflammatory cells accumulate
  • type 2 pneumocytes replace type 1
  • fibrosis follows
250
Q

Phases for DAD

A
  • Exudative phase
  • Organizing phase
  • Resolution
251
Q

Exudative Phase

A
  • DAD
  • first phase, develops over first week following the insult
  • accumulation of inflammatory cells
  • sloughing of type 1 cells
  • can be edema as well
252
Q

Organizing phase

A
  • DAD
  • second phase, second week following injury
  • proliferation of type 2 pneumocytes
  • varying degrees of fibrosis follow q
253
Q

Resolution phase

A
  • DAD
  • third phase
  • those who survive will gradually improve, most likely not to original function b/c of fibrosis that is left
254
Q

Clinical Features of ARDS

A
  • typically present a few hours post-insult with dyspnea, progressive hypoxemia, and diffuse infiltrate on chest x-ray
  • most often will require mechanical ventilation and high levels of O2
  • improvement in mortality rate from 70% 40 yrs ago to 40% recently
  • no specific therapy, supportive care used, reverse underlying cause if possible
255
Q

COPD

A
  • chronic obstructive pulmonary disease
  • patients with both chronic bronchitis or emphysema who show evidence of decreased expiratory flows
  • irreversible
256
Q

Chronic Bronchitis

A
  • defined by symptoms
  • presence of chronic productive cough for >3 months per year over 2 years
  • leading cause is cigarette smoking (>90% of those with disease are smokers)
  • pathology includes hyperplasia of mucus secreting cells
  • thickening of bronchial wall
  • excess mucus in airways
  • chronic PRODUCTIVE cough and dyspnea
  • treatment: flu and pneumonia vaccines, anitbiotics, bronchodilator & anti-imflammatory meds, supplemental oxygen
257
Q

Emphysema

A
  • defined by pathology
  • enlargement of air spaces in alveolar sacs with destruction of bronchial walls
  • no significant fibrosis
  • major cause is cigarette smoking (increased number of neutrophils)
  • damage to elastic tissues which leads to impaired elastic recoil and dilation of bronchioles
  • little relationship between location of the emphysema and its clinical manifestation
258
Q

1% of emphysema patients are deficient in what?

A

alpha-1 anti-trypsin

- most of time emphysema from outside factors causing damage

259
Q

Emphysema clinical features

A
  • most greater than 60 yrs old
  • progressive dyspnea upon exertion
  • patients often have weight loss secondary to increased work of breathing
  • chest hyperinflation
  • no cure, treatment is to stop smoking, oxygen therapy, bronchodilators
  • in end stage, patient can be considered for lung transplantation
260
Q

Asthma

A
  • reversible airway obstruction with increased airway resistance to a variety stimuli
  • airway inflammation common
  • 7% of US population
  • allergy important risk factor
261
Q

Pathogenesis & Pathology of Asthma

A
  • stimuli lead to release of histamine, prostaglandins, leukotrienes from inflammatory cells in lungs
  • these contribute to airway edema, increased mucus secretion, and smooth muscle contractions
  • pathology: loss of bronchial epithelium, inflammation with eosinophils
262
Q

Clinical features of asthma

A
  • occasional or frequent attacks that manifest as cough, chest tightness, wheezing, and dyspnea
  • viral upper respiratory infection most common cause of asthma exacerbations
  • treatment includes bronchodilators, anti-inflammatory drugs
  • 10% of patients do not respond to therapy
263
Q

Pneumothorax

A
  • accumulation of air in the pleural space
  • spontaneous, secondary to trauma, or complication of lung disease or surgery
  • decreased breath sounds
  • larger or symptomatic needs draining via chest tube
264
Q

Pleural Effusion

A
  • accumulation of fluid in pleural space
  • can be serous (simple effusion), bloody (hemorrhagic effusion), or pus-like (empyema)
  • can be cause by elevated hydrostatic pressure in capillaries, low plasma protein, or pleural inflammation or trauma
  • decreased breath sounds
  • severe needs draining via chest tube
265
Q

3 mechanical barriers of the respiratory system

A
  • Nose (traps large particles)
  • Mucociliary Blanket (traps midsized particles)
  • cough (clears airways)
266
Q

Non-specific and immune defense mechanisms respiratory system

A
  • alveolar macrophages (protect from small particles 1-2 microns)
  • neutrophils
  • anti-oxidants
267
Q

Congenital Abnormalities in respiratory systems

A
  • incomplete or defective development of a part or entire lung
  • can be asymptomatic and discovered later in life
  • either a smaller or extra structure
  • most common are bronchial atresia, pulmonary hypoplasia, bronchogenic cyst, pulmonary sequestration
268
Q

diseases involving the bronchi and bronchioles include (3)

A

infection, obstruction, and bronchiectasis (destruction)

269
Q

Infection of bronchi and bronchioles

A
  • central airway: bronchitis
  • peripheral airways: bronchiolitis
  • bronchiolitis typically seen in children (croop)
  • causes include viruses like flu and bacteria strep, and pneumonia
  • main symptoms cough, sputum production or fever
270
Q

Broncial Obstruction

A
  • most commonly caused by aspiration of foreign bodies in children
  • most commonly caused by lung disease or aspiration or thick mucus in adults
  • affects more men
  • pulmonary segment distal to the area of obstruction is susceptible to pneumonia, abscess formation, and bronchiolitis
  • can lead to collapse of lung tissue distal to area of obstruction
271
Q

collapse of lung tissue distal to area of obstruction

A
  • atelectasis
272
Q

Bronchiectasis

A
  • destruction by permanent dilation of airway secondary to destruction of elastic and muscular elements
  • can be secondary to obstruction, infections, or congenital abnormalities
  • manifest by chronic cough with sputum production
  • hemoptysis is common
  • usually long-standing and recurrent infections
273
Q

Pneumonia

A

infection of pulmonary parenchyma (lung tissue)

  • can be caused by bacteria, viruses, fungi, and other organisms
  • symptoms include fever, cough, chest pain, sputum production, and shortness of breath
274
Q

3 categories of pneumonia

A
  • community aquired pneumonia (outside the hospital)
  • nosocomial pneumonia (already hospitalized, in hospital environment)
  • opportunistic pneumonia (represents infection in patients with compromised immune status)
275
Q

types of Community Acquired pneumonia (5)

A
  • bacteria pneumonia
  • mycoplasma pneumonia
  • legionella pneumonia
  • viral pneumonia
  • fungal pneumonia
276
Q

Community acquired bacterial pneumonia

A
  • involves aspiration of organisms from the upper airway, prior viral infections, and immunosuppression
  • early stages involve inflammation of parenchyma and outpouring of leukocytes
  • affected segment of lung becomes firm (“red hepatatization”)
  • over next few days congestion decreases but lung remains firm (“gray hepatatitization”)
  • resolution stage follows
277
Q

empyema

A
  • pleural effusion that can become infected

- complication of pneumonia

278
Q

most community acquired pneumonias are caused by ____. what is treatment?

A
  • streptococcus pneumoniae

- antibiotics and supportive care

279
Q

Mycoplasma Pneumonia

A
  • community acquired
  • gradual onset of respiratory systems and bronchopneumonia
  • typically young adult
280
Q

Legionella pneumonia

A
  • community acquired or nosocomial
  • caused by bacterium legionella pneumophila
  • spreads through water environments
  • multi-lobular involvement and bronchopneumonia
  • symptoms similar to pneumococcal pneumonia
281
Q

Viral Pneumonia

A
  • community acquired
  • measels, varicella rare causes for pneumonia
  • rarely fatal except in immunocompromised hosts
  • influenza can cause pneumonia in previously healthy people and could result in failure of multiple organs and death
282
Q

Fungal Pneumonia

A
  • community acquired

- divided into two types: ones found outdoors and ones that afflict immunocompromised hosts

283
Q

main example of fungal pneumonia that affects immunocompromised hosts

A
  • aspergillosis
284
Q

Blastomycosis

A
  • fungal pneumonia that is community acquired
  • found in the midwest
  • causes infection of the parenchyma and lymph nodes of chest
  • symptoms large range from mild to fatal respiratory failure
285
Q

Nosocomial pneumonia

A
  • hospital pneumonia
  • caused by gram negative organisms or staphylococcus aureus which is gram positive
  • highest risk in a patient a few days after hospitalization
  • highest risk of those on ventillation and in ICU
286
Q

Opportunistic pneumonias (3)

A
  • occurs in immunocompromised hosts
  • Pneumocystis carinii pneumonia/pneumocystis Jiroveci Pneumonia (PJP)
  • Fungal
  • Viral
287
Q

Pneumocystis Jiroveci Pneumonia (PJP)

A
  • occurs in immune-compromised hosts
  • symptoms vary from minimal to severe progressive respiratory failure
  • treatments include antibiotics, corticosteroids, and supportive care
288
Q

Aspergilosis

A
  • fungal opportunistic pneumonia
  • seen in patients with severe neutropenia (low white count) and other immune compromised states
  • manifests by diffuse nodular lesions which invade pulmonary blood vessels (can then spread to other organs)
  • can lead to death, but antifungals to treat
289
Q

Prevention of pneumonia

A
  • vaccine very effective in preventing/reducing severity of pneumococcal pneumonia
  • patients with chronic medical problems and those above 65 should get vaccine
  • influenza vaccine also recommended
  • two vaccines for pneumonia (repeat every 5-10 yrs)
290
Q

Lung Abscess

A
  • localized accumulation of pus in area of destroyed parenchyma
  • most common cause for abscess is aspiration
  • patients typically present with fever, productive cough, and chest pain
  • can be complicated by hemoptysis, empyema, or other infections in the body
  • most often the aspiration results from altered consciousness like alcohol.

Path 404 (5 decks)

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