Renal and Reproductive Disorders Flashcards

1
Q

Acute Kidney Injury: Aetiology and Pathophysiology

A

sudden reduction in glomerular filtration rate
categorised into 3 types:
Prerenal: reduced blood flow to kidneys; decreased glomerular filtration rate.
Intrarenal: kidney tissue damage due to disease.
Postrenal: urine flow blocked after leaving kidneys.

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2
Q

Acute Kidney Injury: clinical manifestations

A

Kidney function decline: decreased glomerular filtration rate, increased serum creatinine and blood urea nitrogen.
Sudden reduction in urine output; possible cessation of urine production.
Prerenal: hypotension, tachycardia
Intrarenal and postrenal: hypertension.
Side pain, potassium retention, swelling due to reduced glomerular filtration rate.

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3
Q

Acute Kidney Injury: Diagnosis

A

Essential tests: blood count, electrolyte levels, renal function, urinalysis.
Helps distinguish acute from chronic kidney disease.

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4
Q

Acute Kidney Injury: Management

A

Tailor treatment to type and cause.
Address underlying cause for recovery.
Renal function recovery may take months; not always complete.
Treatment must match type: Diuretics for intrarenal, but may worsen prerenal.

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5
Q

Chronic Kidney Disease: Aetiology and Pathophysiology

A

Chronic kidney disease develops gradually due to long-standing conditions like diabetes mellitus and hypertension.
Characterized by gradual loss of nephron function, measured by reduced glomerular filtration rate.
Kidneys can adapt; clinical signs of impairment appear only after 70–75% loss of function.

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6
Q

Chronic Kidney Disease: Clinical Manifestations

A

Nitrogenous wastes build up in the blood, leading to uraemia (urine components in the bloodstream).
Early symptoms: hypertension, nocturia, restless legs, hematuria, shortness of breath, fatigue, anorexia, weight loss.
Progression: itchy, dry skin, increased infection risk from scratching.
End-stage kidney disease: fluid and electrolyte imbalances, cardiovascular dysfunction, anemia, platelet dysfunction, gastrointestinal/endocrine issues, skeletal and neurological problems.
Other issues: immune suppression, reduced sex hormone levels, decreased libido, infertility.

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7
Q

Chronic Kidney Disease: Diagnosis

A

Blood tests for full blood count, electrolyte levels, renal and liver function are essential for monitoring disease progression.
Urinalysis may show blood, white blood cells (if infection), and increased protein levels.

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8
Q

Chronic Kidney Disease: Management

A

End-stage kidney disease is incurable; focus on slowing or halting disease progression.
Dialysis is the primary treatment for end-stage kidney disease.

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9
Q

Urinary Tract Infections (UTI): Aetiology and Pathophysiology

A

Kidneys, ureters, bladder, and proximal urethra are sterile, maintained by urine flushing.
Distal urethra has resident microbes; urine becomes contaminated during passage.
Compromised urinary tract defences increase infection risk.
Most urinary tract infections originate from the patient’s bowel flora.
Bacteria enter the urinary tract at the urethral opening and ascend to the bladder.
Hospital-acquired infections often result from urological procedures, especially catheterization.
Females are 30 times more likely to develop urinary tract infections due to shorter urethra and proximity to the anus.
Higher infection rates in older adults due to bladder dysfunction, incontinence, and hormonal changes.
Risk factors include urinary tract obstruction, incomplete voiding, and diabetes mellitus.

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10
Q

Urinary Tract Infections (UTI): clinical manifestations

A

Symptoms of urethritis or cystitis (inflammation of the bladder): pain during urination (dysuria), increased frequency and urgency of urination.

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11
Q

Urinary Tract Infections (UTI): Diagnosis

A

Urine may have an offensive smell, abnormal colour, and cloudy appearance.
Urinary dipstick test may show positive results for blood and nitrite.
Midstream urine sample analysis may reveal leucocytes, high bacteria concentration, nitrite, and blood.

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12
Q

Urinary Tract Infections (UTI): Management

A

Removing or replacing an indwelling catheter often resolves the infection.
Broad-spectrum antimicrobial therapy initiated while awaiting culture results.
Encourage fluid intake to help flush bacteria from the urinary tract.
Urinary alkalisers and warm baths may reduce dysuria.
Cranberry derivatives are gaining acceptance to prevent bacterial adhesion in the urinary tract.

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13
Q

Sexually Transmitted Infections (STI): Aetiology and Pathophysiology

A

acquired through vaginal, anal, and/or oral sex with an infected individual.
Common STIs include herpes, genital warts, hepatitis, HIV/AIDS, chlamydia, gonorrhoea, and syphilis.
These infections cause local tissue damage and inflammation at the entry point.
If untreated, they can lead to chronic inflammation, affecting pelvic organs and potentially causing systemic lesions.

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14
Q

Sexually Transmitted Infections (STI): clinical manifestations

A

STIs can be asymptomatic.
Symptoms usually appear 5–14 days after infection.
Symptoms include cramps, lower abdominal pain, painful urination, painful menstruation, and abnormal vaginal discharge.
Infections may occasionally spread to systemic structures, particularly the joints.

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15
Q

Sexually Transmitted Infections (STI): Diagnosis

A

Diagnosis involves clinical history, physical examination, swabs, urinary polymerase chain reaction tests, syphilis serology, and Pap smear.

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16
Q

Sexually Transmitted Infections (STI): Management

A

Treatment depends on the causative organism.
Antibiotics are effective for bacterial infections.
Antiviral agents reduce genital herpes symptoms but do not cure the infection.
Genital warts can be removed surgically or treated with cryotherapy (cold or freeze therapy), laser ablation, or electrocautery (using heat from an electrical current)
Care plan should be non-judgmental, reduce anxiety, and maintain privacy.

17
Q

Polycystic Ovary Syndrome: Aetiology and Pathophysiology

A

Caused by endocrine imbalance with elevated estrogen, testosterone, luteinizing hormone, and reduced follicle-stimulating hormone.
Exact cause unclear; likely a combination of genetic and environmental factors.
Leads to numerous ovarian follicles, excess estrogen, ovarian enlargement, and irregular egg release.

18
Q

Polycystic Ovary Syndrome: clinical manifestations

A

Symptoms: Infrequent or prolonged menstrual periods, elevated male hormone levels.
Typically diagnosed during adolescence when symptoms appear.
Other symptoms: amenorrhea (absence of menstruation), acne, obesity, excessive hair growth in male-pattern areas (face, chest, back)

19
Q

Polycystic Ovary Syndrome: Diagnosis

A

Diagnosis includes clinical history, physical examination, pelvic ultrasound, and laparoscopy.
Blood tests to assess gonadotropin and ovarian hormone levels.
Metabolic profiles (glucose tolerance, insulin resistance, lipid levels) may be evaluated.

20
Q

Polycystic Ovary Syndrome: Management

A

Treatment individualized based on symptoms, fertility goals, and complication prevention.
Options: lifestyle changes for weight reduction, hormonal therapy to regulate menstruation and reduce androgen production.
Ovulation-promoting medications may be prescribed for women who wish to conceive.

21
Q

Breast Cancer: Aetiology and Pathophysiology

A

Most breast cancers originate from epithelial cells lining milk ducts and lobules
.
Cancers in milk ducts can become invasive, spreading to surrounding breast tissue, lymphatic and blood vessels.

Locally advanced breast disease occurs when cancer invades skin, chest wall, or lymph nodes, potentially causing lymphoedema.

Metastatic breast cancer refers to the spread of cancer cells to distant tissues via bloodstream and lymphatic system.

Specific gene mutations are strongly linked to increased breast cancer risk

22
Q

Breast Cancer: Risk Factors

A

Age, female gender, long reproductive life, few children, late first pregnancy, high saturated fat diet, obesity, alcohol consumption, urban living, ethnicity, genetics, family history, radiation exposure, hormone therapy.

23
Q

Breast Cancer: clinical manifestations

A

Common symptoms: Lump in the breast (can be painful), changes in nipple position/orientation, alterations in breast skin colour/texture, abnormal nipple discharge (clear or blood-stained)

24
Q

Breast Cancer: Diagnosis

A

Involves health history, physical examination, mammography, and possibly ultrasound.
Biopsy (fine-needle aspiration or open procedure) is performed for histological and cytological examination

25
Q

Breast Cancer: Management

A

Depends on tumor histology, staging, patient’s age, and health history.
Treatment options: Surgery, radiation therapy, reconstruction surgery (immediate or delayed), chemotherapeutic agents, hormone therapy, immunotherapy.
Continuous psychological support and regular follow-up assessments are essential.

26
Q

Benign Prostatic Hyperplasia: Aetiology and Pathophysiology

A

Benign prostatic hyperplasia is a common chronic condition in men, characterized by remodelling of prostatic tissue.
Involves hyperplasia (increase in cell number) and hypertrophy (increase in cell size) in advanced stages.
Enlarged prostate constricts the proximal urethra, disrupting urine flow from the bladder.
Results in uncoordinated bladder muscle contractions, leading to an overactive bladder and incomplete voiding.
Lower urinary tract symptoms develop as a result of these changes.
Prevalence increases with age: 50% in men aged 50–60 years, 90% in men over 80 years.
Influenced by androgen levels and their interaction with prostate androgen receptors.

27
Q

Benign Prostatic Hyperplasia: clinical manifestations

A

Asymptomatic until the enlarged prostate obstructs urine flow.
Symptoms include reduced urine flow, painful urination, urinary retention, urgency, and urine reflux.

28
Q

Benign Prostatic Hyperplasia: Diagnosis

A

Diagnosis includes health history, symptom scoring, and digital rectal examination to assess prostate size, texture, and tenderness.
Additional tests: Urine microbiology, blood tests (renal function, prostate-specific antigen), FBC, creatinine levels, X-ray, ultrasound, and prostate biopsy.

29
Q

Benign Prostatic Hyperplasia: Management

A

Management depends on symptom severity and complications.
Mild cases require ongoing monitoring.
Medications can reduce prostate size, decrease muscle contraction, alleviate obstruction, and improve urinary flow.
Surgical intervention may be needed for urinary retention, recurrent infections, bladder stones, blood in urine, or renal impairment.

30
Q

Prostate Cancer: Aetiology and Pathophysiology

A

Causes of prostate cancer are multifactorial: genetic predisposition, ethnicity, hormonal levels, and dietary factors (high in saturated fats).
Most prostate cancers are adenocarcinomas originating in glandular tissue; others develop from epithelial lining or neuroendocrine stem cells.
Mutations in prostate cells may metastasize to other body parts, but not always.
Highly prevalent, second to lung cancer in cancer-related deaths among men.
Primarily affects older men over 65; rare in men under 50.

31
Q

Prostate Cancer: clinical manifestations

A

Symptoms: Weak urine stream, urgency or hesitancy to urinate, frequent nighttime urination, incomplete bladder emptying

32
Q

Prostate Cancer: Diagnosis

A

Often detected through screening.
Involves health history, symptom scoring, and digital rectal examination to assess prostate size and texture.
Definitive diagnosis: Transrectal ultrasound-guided prostate biopsy.
Additional tests: Urinalysis (for red/white blood cells, bacteria), blood tests (elevated prostate-specific antigen levels).

33
Q

Prostate Cancer: Management

A

Tailored to patient’s age, health, and preferences.
Treatment options: Surgery, radiation therapy, hormonal manipulation.
Hormone therapy used for advanced cancer or to shrink tumors before radiation; involves luteinising hormone-releasing hormone agonists (to prevent testicles from releasing testosterone) or anti-androgens (to stop testosterone from reaching cancer cells)