B. Umweltschutz. Wаs kаnn, sоll, dаrf, muss gemacht werden, um die Umwelt zu schützen? Schreiben Sie Sätze im Passiv Präsens (PRESENT TENSE) mit Mоdalverben. Beispiel: Papier wieder verwenden / können Papier kann wieder verwendet werden. alternative Energien fördern / müssen Atоmenergie verbieten / sollen Chemikalien reduzieren / müssen Abfall kompostieren / können Regenwälder schützen / sollen
III. Lesen Glоbаle Prоbleme. Sо hаben drei Studierende in Berlin die Frаge „Was sind deiner Meinung nach die drei größten Probleme auf der Welt?“ beantwortet. Lesen Sie Ihre Antworten und beantworten Sie die Fragen. (8 Punkte) lara: Es gibt mehrere Probleme auf der Welt. Ich würde mal sagen, die drei größten Probleme sind Umweltverschmutzung, Arbeitslosigkeit und Terrorismus. Ich denk’ auch hier in Berlin ist das größte Problem die Arbeitslosigkeit. Es gibt viele Menschen, die Arbeit suchen aber keine finden. Und Gewalt oder Terror von feindlichen (hostile) Gruppen – davor muss man richtig Angst haben. Das kann überall passieren. Die Arbeitslosigkeit bekämpfen (fight against) ist schwierig. Es müßte natürlich mehr Arbeitsplätze geben, aber wie man das macht, ist eine große Frage. niels: Die drei größten Probleme der Welt sind sicherlich neben vielen anderen, Umweltverschmutzung, Geldmangel (lack of money) und Rassismus. Das Problem mit Geld wird an Berlin deutlich. Die Stadt hat kein Geld mehr. Sie kann kein Geld in Kultur oder Bildung (education) investieren. Das schafft ein großes Problem und bringt andere Probleme mit sich. Ich glaube aber, man kann sehr viele Dinge für die Umwelt tun, zum Beispiel, Zeitungen sammeln und wiederverwerten (reuse), Glasflaschen sammeln und recyceln, mit Stoffbeuteln (cloth bags) einkaufen gehen, statt Plastiktüten zu benutzen, beim Zähneputzen das Wasser nicht laufen lassen … und vieles mehr. jule: Wenn man sich momentan umschaut, dann denk’ ich Umweltverschmutzung ist ein ernsthaftes Problem, und auch Krankheiten wie Ebola und Aids, und schließlich Terroranschläge (terror attacks), die sehr aktuell sind. Ich sehe, dass Ebola in Afrika sehr stark zugenommen hat und dass die medizinische Versorgung noch nicht das bringt, was sie bringen könnte. Vor Terroranschlägen muss man sich auch fürchten – zu Hause und wenn man reist. Man fühlt sich nicht so sicher. Welche Probleme hat die Stadt Berlin? Nennen Sie drei Dinge, die Niels vorschlägt, um die Umwelt zu schützen. Was ist Jules Meinung über Ebola und Aids? Macht Lara Vorschläge, wie man die Arbeitslosigkeit bekämpfen kann?
Nephritic Syndrоme (Study Outline) 1. Bаckgrоund Definitiоn: A glomerulаr inflаmmatory syndrome characterized by hematuria, variable proteinuria, reduced GFR, and hypertension. Pathophysiology: Immune-mediated inflammation of the glomeruli → impaired filtration barrier → RBC leakage, decreased GFR, sodium/water retention. Common causes (high-yield): Post–streptococcal glomerulonephritis (after group A strep pharyngitis/impetigo). IgA nephropathy (Berger disease) − recurrent episodes after URI. Henoch–Schönlein purpura (IgA vasculitis). Rapidly progressive glomerulonephritis (RPGN): Anti-GBM disease (Goodpasture). ANCA-associated vasculitides (GPA, MPA). Lupus nephritis (SLE). 2. History Hematuria (tea- or cola-colored urine) — hallmark. Recent infections: strep throat or skin infection (10–21 days prior). Edema: periorbital, peripheral (mild to moderate). Hypertension due to fluid retention. Oliguria or reduced urine output. Systemic symptoms depending on cause: IgA: gross hematuria immediately after URI. Vasculitis: constitutional symptoms, sinus disease, pulmonary complaints (Goodpasture → hemoptysis). Lupus: rash, arthralgias. 3. Exam Findings Edema: periorbital swelling common in post-strep GN. Hypertension (very common). Volume status: mild fluid overload signs. Rash or purpura (IgA vasculitis). Pulmonary findings: hemoptysis in Goodpasture. Signs of systemic autoimmune disease (malar rash, arthritis). 4. Making the Diagnosis Urinalysis (high-yield): Hematuria with RBC casts (diagnostic hallmark). Proteinuria (usually
Hypercаlcemiа (Study Outline) 1. Bаckgrоund Definitiоn: Serum calcium abоve the lab reference range (often >10.5 mg/dL). Pathophysiology: Results from increased bone resorption, increased GI absorption, or decreased renal excretion of calcium. Divided into PTH-dependent vs. PTH-independent causes (high-yield classification). Major etiologies: PTH-dependent: Primary hyperparathyroidism (most common outpatient). Tertiary hyperparathyroidism (long-standing CKD). PTH-independent: Malignancy-associated hypercalcemia (most common inpatient). PTHrP-producing tumors, bone metastases, lymphoma (↑ calcitriol). Vitamin D excess. Granulomatous disease (sarcoidosis → ↑ 1-α–hydroxylase). Medications: thiazides, lithium. Endocrine disorders: hyperthyroidism, adrenal insufficiency. Misc: Milk-alkali syndrome, immobilization. 2. History Classic symptoms (stones, bones, groans, psychiatric overtones): Kidney stones, polyuria, polydipsia. Bone pain, fractures (in severe disease). Abdominal pain, constipation, nausea. Fatigue, depression, cognitive changes, confusion. Etiology clues: Malignancy: weight loss, night sweats. Hyperparathyroidism: history of kidney stones, bone pain, osteoporosis. Granulomatous disease: respiratory symptoms, uveitis. Medication use: thiazides, lithium, supplements. 3. Exam Findings General: dehydration signs (polyuria → volume loss). Neuro: lethargy, slow mentation, AMS in severe cases. GI: slowed bowel sounds, constipation. Renal: flank pain if nephrolithiasis; CVA tenderness if obstruction. Endocrine clues: thyroid enlargement (hyperthyroidism), lymphadenopathy (malignancy), sarcoid skin lesions. Bone tenderness in advanced disease. 4. Making the Diagnosis Initial labs: Total and ionized calcium (corrected Ca²⁺ if albumin low). PTH level → major branch point: High or inappropriately normal PTH → PTH-dependent causes. Low PTH → PTH-independent (malignancy, vitamin D excess, granulomatous disease). Additional labs based on PTH status: If PTH high: Serum phosphate low (typical of primary hyperparathyroidism). If PTH low: PTHrP (malignancy). 25-OH vitamin D (toxicity). 1,25-OH₂ vitamin D (granulomatous disease, lymphoma). Renal function to assess for CKD-related disorders. Urine calcium: helps differentiate hyperparathyroidism vs. familial hypocalciuric hypercalcemia. Imaging: Consider malignancy screening if suspicion high. Bone density in chronic hyperparathyroidism. Gold Standard: Lab-confirmed elevated calcium with evaluation of PTH to determine etiology. 5. Management (Exam Concepts) (No real-time treatment recommendations or dosing — conceptual principles only.) General principles: Identify and address underlying cause. Ensure adequate hydration conceptually (volume status is key). Avoid nephrotoxins; adjust renally cleared medications. Indications for urgent management (exam clues): Severe hypercalcemia with neurologic symptoms. Calcium levels significantly above normal with dehydration. Conceptual therapeutic approaches: Volume management: correct volume depletion first (concept-level). Bone resorption reduction: antiresorptive therapy concepts sometimes tested (no specifics). Address PTH-independent causes: Malignancy-associated hypercalcemia: treat underlying cancer conceptually. Granulomatous disease: immunologic modulation concepts. Renal replacement therapy: considered conceptually for severe, refractory cases or in advanced renal failure. Monitoring: Serial calcium levels. Renal function and urine output. ECG monitoring in severe cases (short QT interval is classic). Referral: Endocrinology for hyperparathyroidism, unexplained hypercalcemia, or suspected malignancy-associated processes. QUESTION A 60-year-old man presents to his primary care provider with fatigue, constipation, and mild confusion for the past two weeks. He also reports a 10-lb unintentional weight loss over the past month and increasing thirst. He has no significant past medical history and takes no medications or supplements. Vitals are normal. Physical exam reveals mild dehydration but no lymphadenopathy or palpable masses. Laboratory studies show: Total calcium: 13.2 mg/dL (reference: 8.5–10.5) Albumin: 4.2 g/dL Serum creatinine: 1.3 mg/dL (baseline: 1.0) Parathyroid hormone (PTH): 8 pg/mL (reference: 15–65) PTH-related peptide (PTHrP): elevated 25-hydroxy vitamin D: normal Which of the following is the most likely cause of this patient’s hypercalcemia? A) Primary hyperparathyroidismB) SarcoidosisC) Malignancy-associated hypercalcemiaD) Vitamin D toxicity
Pоlycystic Kidney Diseаse – Autоsоmаl Dominаnt (ADPKD) (Study Outline) 1. Background Definition: A genetic disorder causing progressive formation and enlargement of numerous kidney cysts → renal enlargement, loss of function, and eventual CKD/ESRD. Genetics: Autosomal dominant inheritance. Mutations in PKD1 (≈85%) or PKD2 (≈15%); PKD1 associated with earlier, more severe disease. Pathophysiology: Cyst formation from renal tubules → expansion → compression of normal parenchyma → ischemia and fibrosis. Epidemiology: Most common life-threatening monogenic kidney disorder. Presents in adulthood (often ages 20–40). Associated extrarenal manifestations: Hepatic cysts (most common). Pancreatic and splenic cysts. Cerebral aneurysms (berry aneurysms). Cardiac valve abnormalities (MVP, AR). Diverticulosis, abdominal wall/inguinal hernias. 2. History Flank or abdominal pain: due to cyst enlargement, bleeding, or infection. Hematuria: microscopic or gross; often from cyst rupture. Hypertension: very common early due to RAAS activation. Recurrent UTIs or pyelonephritis. Nephrolithiasis (uric acid or calcium oxalate). Family history: first-degree relatives frequently affected. Progressive symptoms of CKD later (fatigue, nocturia, edema). 3. Exam Findings Abdominal masses: bilateral, palpable enlarged kidneys (important exam clue). Hypertension (often severe). Signs of CKD: edema, pallor, asterixis (later stages). Liver enlargement if significant hepatic cysts. Neurologic red flags: severe headaches (possible aneurysm). 4. Making the Diagnosis Labs: Proteinuria (usually mild), possible hematuria. Progressive elevation in BUN/Cr with disease advancement. Imaging (high-yield): Ultrasound = first-line test Shows multiple bilateral renal cysts of varying sizes. CT/MRI: used if ultrasound inconclusive. Diagnostic criteria (age-based, classic): ≥3 cysts total (unilateral or bilateral) if age