Endocrine 1 Flashcards
(181 cards)
1
Q
✂️The initial treatment of DKA is …..
DKA = Diabetic Ketoacidosis
A
✅ IV fluids with short-acting insulin
➡️ Fluids first to restore perfusion
➡️ Then insulin to correct hyperglycemia and ketoacidosis
2
Q
What are the key clinical features of DKA⁉️
A
🚩 Nausea, vomiting, abdominal pain
🚩 Fruity breath odor, dyspnea, tachypnea (Kussmaul breathing)
🚩 Tachycardia, hypotension, lethargy
2
Q
What laboratory findings are characteristic of DKA⁉️
A
🚩Hyperglycemia (300–600 mg/dL)
🚩 Positive serum/urine ketones
🚩 Metabolic acidosis (low pH, low bicarbonate)
2
Q
What are the major steps in DKA management⁉️
A
🔹IV fluids ➡️ restore volume
🔹 Insulin ➡️ short-acting to reduce glucose/ketones
🔹 Potassium ➡️ added if low or normal
🔹 Bicarbonate ➡️ only if pH < 7.0
🔹 Identify and treat the cause (e.g. infection, infarction)
3
Q
What are serious complications of DKA⁉️
A
🚨 Cerebral edema — most serious
⚠️ Others: ARDS (acute respiratory distress syndrome), GI bleeding, venous thrombosis
3
Q
Which antidiabetic drug causes weight loss⁉️
A
✅ Liraglutide
🧠 A GLP-1 (glucagon-like peptide-1) receptor agonist
➡️ Increases insulin, suppresses glucagon, slows gastric emptying
💡 Associated with mild weight loss
⚠️ Main side effect = nausea
3
Q
Which antidiabetic drugs are associated with weight gain⁉️
A
⛔ Insulin & insulin analogs
⛔Sulfonylureas & non-sulfonylurea secretagogues (e.g., Repaglinide)
⛔ Thiazolidinediones (e.g., Rosiglitazone)
4
Q
What is the effect of sitagliptin on weight⁉️
A
🧠 Weight neutral
✅ Does not cause weight gain
✅ Does not cause weight loss
📝sitagliptinis a DPP-4 inhibitor (dipeptidyl peptidase-4)
5
Q
What is the treatment of subacute thyroiditis⁉️
A
✅ NSAIDs or aspirin for pain/inflammation
✅ Glucocorticoids for severe/refractory cases
✅ Beta-blockers for thyrotoxic symptoms
⛔ Antithyroid drugs have no role
➡️ Use thyroid hormone replacement if hypothyroid phase is prolonged
5
Q
What are the 3 phases of subacute thyroiditis progression⁉️
A
- Thyrotoxic phase → ↑ T3/T4
- Hypothyroid phase → ↓ thyroid hormones
-
Recovery phase → return to euthyroid state
⚠️ 15% may develop permanent hypothyroidism.
6
Q
How can subacute thyroiditis be differentiated from Graves’ disease and toxic adenoma on scan⁉️
A
📸 Subacute thyroiditis → low/absent uptake
📸 Graves’ disease → diffuse increased uptake
📸 Toxic adenoma → focal increased uptake
6
Q
What is the role of the radioactive iodine uptake test in subacute thyroiditis⁉️
A
🔬 Low or absent uptake due to thyroid inflammation and hormone leakage
✅ Helps differentiate from Graves’ disease or toxic adenoma (which show increased uptake)
7
Q
🧠Key clues to diagnose a case of Subacute thyroiditis (de Quervain’s thyroiditis)
A
🔹Post-viral onset
🔹Painful, tender thyroid
🔹Transient hyperthyroidism(e.g. tremor, tachycardia)
🔹Elevated ESR
🔹↓ TSH
🔹Decreased RAIU due to release (not overproduction) of thyroid hormone
8
Q
What is the next step if TSH is elevated in suspected hypothyroidism⁉️
A
➡️ Measure free T4 (FT4)
🔹 FT4 low → Primary hypothyroidism
🔹 FT4 normal → Mild hypothyroidism
8
Q
What is the diagnosis if TSH is high and FT4 is low⁉️
A
✅ Primary hypothyroidism
9
Q
What is the diagnosis when TSH is high, FT4 is low, and TPO antibodies are positive⁉️
A
✅ Autoimmune hypothyroidism → Start T4 treatment.
9
Q
How is mild hypothyroidism managed if TPO antibodies are positive or patient is symptomatic⁉️
A
✅ Start T4 treatment
10
Q
What is the next step when TSH is normal but pituitary disease is suspected in hypothyroidism⁉️
A
➡️ Measure FT4
🔻 If low → Evaluate pituitary function (rule out drug effects, sick euthyroid, etc.)
11
Q
A
11
Q
What is the next step in a patient with low TSH and normal FT4⁉️
A
➡️ Measure FT3
🔹 If high → ✅ T3 toxicosis
🔹 If normal → ✅ Subclinical hyperthyroidism → Follow-up in 6–12 weeks
11
Q
What does low TSH with elevated FT4 indicate, and what is the next step⁉️
A
✅ Primary thyrotoxicosis
➡️ Look for Graves’ disease features (e.g. ophthalmopathy, dermopathy, diffuse goiter)
12
Q
What if Graves’ disease features are absent in primary thyrotoxicosis( low TSH with elevated FT4 )⁉️
A
➡️ Check for multinodular goiter or toxic adenoma
🔹 If present → ✅ Toxic nodular hyperthyroidism
🔹 If absent → Measure radionuclide uptake
12
Q
What does low radionuclide uptake suggest in thyrotoxicosis⁉️
A
✅ Destructive thyroiditis,
or
✅iodine excess,
or
✅hormone ingestion
13
Q
What are possible causes if radionuclide uptake is normal or high in thyrotoxicosis⁉️
A
✅ Graves’ disease
✅ Toxic nodular hyperthyroidism
✅ TSH-secreting pituitary adenoma (if TSH is inappropriately normal or high)
13
What is a **major side effect** of **bisphosphonates** used in the treatment of osteoporosis⁉️
✅ **Jaw osteonecrosis**
⚠️ Other side effects include:
🔹 Esophageal irritation
🔹 Atypical femoral fractures
14
What is the **correct way** to take oral **bisphosphonates** (e.g. alendronate) to reduce side effects⁉️
✅ Take with a **full glass of water**
✅ Remain **upright for ≥30 minutes**
💡 Reduces risk of esophageal irritation
14
✂️In **Pre-existing esophageal disorders**(e.g. strictures)..... is contraindicated to treat osteoprosis.
**bisphosphonates**
💡As bisphosphonate causes esophageal irritation.
15
A patient with **low TSH** and a “**cold**” thyroid nodule on RAIU scan — what is the **best next step** in management⁉️
✅ **Ultrasound-guided fine needle aspiration (FNA)**
🧠 “Cold” nodules are non-functioning and suspicious for **malignancy**, requiring cytologic evaluation
15
What is the **significance** of a “**cold**” nodule on radionuclide scan⁉️
⚠️ **Non**-functioning nodule with low uptake
🔻 Higher risk of **malignancy**
➡️ Requires **FNA biopsy**
16
When is **radionuclide thyroid scan** indicated in the evaluation of a thyroid **nodule**⁉️
✅ **When TSH is low**
🧠 Differentiates:
▪️ **Hot nodule** = functioning, rarely malignant
▪️ **Cold nodule** = non-functioning, suspicious
17
What is the **role of thyroidectomy** or **anti-thyroid drugs** in a patient with a cold nodule⁉️
⛔ **Not first-line**
✅ Only indicated after **malignancy is confirmed**
➡️ Cold nodules → FNA first
18
What is the **first step** in evaluating a **thyroid nodule** detected by palpation or imaging⁉️
✅ Take patient **history**, perform **physical exam**, and measure **serum TSH**
19
What is the **next step** if **TSH is low** in a patient with thyroid **nodule**⁉️
➡️ **Perform radionuclide scan**
🔹 **“Hot” nodule (functioning)** → treat hyperthyroidism
🔹 “**Cold” nodule (non-functioning)** → suspicious → ➡️ FNA
20
What is the **next step** if **TSH is normal or high** in a patient with a thyroid **nodule**⁉️
➡️ **Proceed to diagnostic ultrasound and lymph node (LN) assessment**
🔸 >1 cm or suspicious features → **FNA**
🔸 <1 cm with no features → **follow-up**
21
What are **sonographic features** associated with **thyroid malignancy**⁉️
* **Hypoechogenicity**
* **Microcalcifications**
* **Irregular, microlobulated margins**
* **Solid consistency**
* **Taller-than-wide shape on transverse view**
22
What patient **history** and **physical exam features** suggest **thyroid malignancy**⁉️
🧠 **History:**
* Age > 65
* Male gender
* Childhood head/neck irradiation
* Family history of thyroid cancer
🧠**Physical exam:**
* Rapidly growing neck mass
* Vocal cord paralysis, hoarseness
* Fixed nodule
* Lateral cervical lymphadenopathy
23
What are common **benign and malignant classifications** of **thyroid nodules**⁉️
🔹 **Benign:**
Thyroid adenomas, cysts
🔹 **Malignant:**
* Carcinomas (papillary, follicular, anaplastic, medullary)
* Lymphoma
* Metastases
23
What are the **key clinical and laboratory** features used to diagnose **primary hyperaldosteronism(Conn Syndrome)**⁉️
🔍**Resistant hypertension** (despite 3+ antihypertensives
🔍**Hypokalemia** (often unexplained)
Metabolic alkalosis
🔍**Suppressed plasma renin activity**
🔍**Elevated plasma aldosterone concentration**
🔍**Aldosterone-to-renin ratio (ARR > 750 pmol/L**
🧠**Confirmatory tests:**
▫️ Saline suppression test
▫️ CT scan of adrenals
▫️ Adrenal vein sampling (if surgery is considered)
23
What is the most likely **diagnosis** in a patient with **elevated aldosterone:renin ratio and normal cortisol**⁉️
✅ **Adrenal adenoma secreting aldosterone**
💡 Aldosterone-producing adenomas are a cause of primary hyperaldosteronism
24
What is the **pathognomonic** clinical feature of **primary hyperaldosteronism**⁉️
⚠️ **Hypokalemic hypertension**
🧠 **Other features:** metabolic alkalosis → muscle cramps, weakness
25
What **test confirms** the diagnosis of **primary hyperaldosteronism**⁉️
**Saline infusion test**
➡️ **Positive** if aldosterone remains elevated after saline load
26
What is the **next step** after biochemical confirmation of **primary hyperaldosteronism**⁉️
📸 **CT scan of the adrenal glands**
➡️ To differentiate between **adenoma** and **bilateral hyperplasia**
26
What is the **initial fluid** of choice for a hemodynamically **unstable** patient with **diabetic ketoacidosis (DKA)**⁉️
✅ **0.9% saline (normal saline)**
💡 First-line fluid resuscitation to restore intravascular volume
27
When is **potassium** added in the management of **DKA**⁉️
✅ **When serum potassium < 5–5.2 mmol/L**
⚠️ Even if initial K⁺ is normal/high, insulin will lower it — monitor closely
⛔ Not needed immediately if K⁺ ≥ 5.2
27
When is **bicarbonate** used in **DKA management**⁉️
⛔ Only if **pH < 7.0**
💡 Not indicated for pH ≥ 7.0 due to lack of benefit and risk of complications
28
When is **0.45%** (half-normal) saline used in **DKA**⁉️
✅ Used **after** initial resuscitation
➡️ Once patient is hemodynamically stable and urine output is adequate
28
Is **3% (hypertonic) saline** used in **DKA**⁉️
⛔ **No — not indicated in DKA**
⚠️ Reserved for cases like severe symptomatic hyponatremia or cerebral edema
29
What does **a thyroid nodule** that uptakes radioactive iodine on a scan **(“hot” nodule)** suggest⁉️
✅ **It is probably benign**
💡 “Hot” nodules are functioning and rarely malignant
30
Are most **incidental** thyroid nodules **malignant**⁉️
⛔ **No** — most incidental nodules are benign
31
What is the **first step** in the evaluation of a newly found **thyroid nodule**⁉️
✅ **History, physical exam, and TSH level**
📌TSH guides whether radionuclide scan or ultrasound is next
32
When should a **radionuclide thyroid scan** be used in nodule evaluation⁉️
✅ Only when **TSH is suppressed**
💡 Helps distinguish between “hot” (functioning) and “cold” (non-functioning) nodules
32
Should all thyroid nodules undergo **fine-needle aspiration (FNA) biopsy**⁉️
⛔ **No** — only nodules with suspicious features or appropriate size on ultrasound should be biopsied
33
A patient with **high calcium** (14.5 mg/dL), **low phosphate** (1.2 mg/dL), and **low PTH** likely has what diagnosis⁉️
✅ **Hypercalcemia of malignancy**
🧠 Often due to **PTHrP secretion** (e.g., squamous cell carcinoma of the lung)
➡️ Mimics PTH effect: ↑Ca²⁺, ↓PO₄³⁻, ↓PTH
34
What distinguishes **hypercalcemia of malignancy** from **primary hyperparathyroidism**⁉️
🔹 **Primary hyperparathyroidism** → ↑PTH
🔹 **Malignancy-related hypercalcemia** → ↓PTH due to negative feedback from high calcium
35
How does **hypercalcemia** present clinically⁉️
⚠️ Fatigue, constipation, anorexia, vomiting
⚠️ Altered mental status, short QT interval, nephrolithiasis, arrhythmias
💡 Can range from asymptomatic to life-threatening
## Footnote
🧠 **Mnemonic**: “Stones, Bones, Groans, Thrones, and Psychiatric Overtones”
❄️ **Stones**>> Kidney stones (nephrolithiasis)
💀**Bones**>> Bone pain (due to bone resorption)
🤢 **Groans** >>GI symptoms: constipation, nausea, abdominal pain, peptic ulcers
🚽 **Thrones**>> Polyuria, dehydration (due to nephrogenic diabetes insipidus)
😵 **Psychiatric Overtones**>> Lethargy, confusion, depression, psychosis
36
What **lab pattern** is seen in vitamin D excess vs deficiency⁉️
🔸 **Vitamin D excess:** ↑Calcium, ↑Phosphate, ↓PTH
🔸 **Vitamin D deficiency:** ↓Calcium, ↑PTH
36
What defines **hypercalcemia** and how is it **corrected with albumin**⁉️
✅ Serum **calcium > 10.5 mg/dL**
➡️ If albumin < 4.1 g/dL, **corrected Ca = measured Ca + 0.8 × (4.1 - albumin)**
37
What is the **first step** in the evaluation of hypercalcemia⁉️
**Measure PTH**
➡️ **High/normal PTH** → PTH-mediated
➡️ **Low PTH** → Non-PTH causes (e.g., malignancy, vitamin D excess)
38
What are the **PTH-mediated causes of hypercalcemia**⁉️
✅ **Primary hyperparathyroidism**
✅ **Familial hypocalciuric hypercalcemia (FHH)**
➡️ Both have ↑Ca²⁺ and ↑/N PTH
💡 FHH = benign; caused by abnormal calcium sensing receptors
38
What are the **non–PTH-mediated causes** of hypercalcemia⁉️
⛔ **PTH is low**
🔹 Malignancy (e.g., PTHrP, bone mets, multiple myeloma)
🔹 Excessive vitamin D (granulomatous diseases, lymphoma)
🔹 Excess calcium intake (milk-alkali syndrome, TPN)
39
What is the **most common** cause of **asymptomatic hypercalcemia** in **healthy** individuals⁉️
✅ **Primary hyperparathyroidism**
➡️ Often due to **adenoma** (80%)
➡️ Check PTH, serum/urine calcium, bone density, kidney function
40
What is the **treatment** for severe hypercalcemia⁉️
✅ **IV hydration with 0.9% saline** (4–6 L/day)
✅ **Bisphosphonates**
✅ **Calcitonin**
✅ **Denosumab or dialysis** (if CKD)
41
✂️In **subacute thyroiditis**.The radioactive iodine uptake test is expected to show.....
**low uptake**
## Footnote
📝Because the thyroid is not actively making new hormone, a radioactive iodine uptake (RAIU) test would show low uptake.
📝This finding helps distinguish subacute thyroiditis from other causes of hyperthyroidism, like Graves' disease.
42
What is the **most likely finding** on a radioactive iodine uptake (RAIU) scan in subacute (de Quervain) thyroiditis⁉️
✅ **Low uptake**
🧠 Hormone elevation is due to destruction of follicles, not increased synthesis
➡️ Helps differentiate from Graves' or toxic adenoma
43
What are **key RAIU findings** in other causes of **thyrotoxicosis**⁉️
📌 **Graves’ disease** → Elevated diffuse uptake
📌 **Toxic adenoma** → Elevated focal uptake
📌 **Subacute thyroiditis** → Low uptake
📌 **Factitious thyrotoxicosis** → Low uptake
44
What are the **two most common causes** of hypercalcemia overall⁉️
1. **Primary hyperparathyroidism**
2. **Malignancy** (e.g., PTHrP, bone mets)
🧠 Together account for >90% of hypercalcemia cases
45
What **features** help **distinguish** malignancy-related hypercalcemia from primary hyperparathyroidism⁉️
🔻 **Malignancy:** acute, symptomatic, weight loss, cachexia, low PTH
✅ **Primary hyperparathyroidism:** often asymptomatic, elevated/normal PTH
46
Which **lab tests** help determine the cause of hypercalcemia⁉️
🔍**PTH**
🔍**PTHrP**
🔍**Phosphate**
🔍**Vitamin D** (25-OH & 1,25-OH forms)
46
What are the **key symptoms** to diagnose **pheochromocytoma**⁉️
🔹 **Severe paroxysmal hypertension** (e.g., 220/150 mmHg)
🔹 **Headaches** (frequent, pounding)
🔹 **Palpitations**
🔹 **Tachycardia**
🔹 **Anxiety or panic-like episodes**
🔹 **Sweating** (diaphoresis)
🔹 May also present with **flushing** or **tremors**
47
What is the **best initial diagnostic test** for pheochromocytoma⁉️
✅ **Measure plasma or 24-hour urine metanephrines**
💡 Elevated metanephrines confirm catecholamine excess
48
✂️BP comparison upper vs lower limbs help diagnosing.....
| BP= blood pressure
**coarctation of aorta**
49
What is the **next step** after **confirming elevated metanephrines** in **pheochromocytoma**⁉️
📸 **Abdominal CT or MRI**
➡️ Localizes the adrenal tumor
50
What is the **most common cardiac dysfunction** seen in patients with **carcinoid syndrome**⁉️
✅ **Tricuspid insufficiency** (tricuspid regurgitation)
🧠 Due to serotonin-induced fibrosis affecting right-sided heart valve
51
Why **doesn't** carcinoid syndrome affect the **left side** of the heart⁉️
🔍Serotonin and other vasoactive substances secreted by carcinoid tumors are **inactivated in the lungs** by monoamine oxidase (MAO) enzymes before they can reach the left side of the heart.
➡️ **Left heart is protected unless there is a right-to-left shunt**
52
What are the **classic symptoms** of carcinoid syndrome⁉️
🔹 **Flushing**
🔹 **Diarrhea**
🔹 **Wheezing**
🔹 **Right-sided valvular heart disease**
⚠️ May also present with pellagra (niacin deficiency)
53
How is **carcinoid syndrome diagnosed**⁉️
📎**24-hour urine 5-HIAA** (serotonin metabolite)
📸 **CT scan** → tumor localization
📡 **Octreoscan** → detect metastasis
📎**Echocardiography** → assess valvular damage
54
What is the **treatment** for **carcinoid syndrome**⁉️
✅ **Octreotide** → symptom control
✅ **Surgical resection** → definitive treatment of primary tumor or metastases
55
What are the **microvascular** complications of diabetes mellitus⁉️
🔹 **Retinopathy**
🔹 **Macular edema**
🔹 **Neuropathy** (mono-, poly-, autonomic)
🔹 **Nephropathy** (e.g., albuminuria)
🧠Eye, nerves,kidney
56
✂️**Macrovascular** complications of diabetes include.....
🔍**Coronary artery disease**
🔍**Cerebrovascular disease**
🔍**Peripheral arterial disease**
57
What are **non-vascular** complications of diabetes mellitus⁉️
🧠 **Gastroparesis**
🧠 **Recurrent infections**
🧠 **Skin changes**
🧠 **Hearing loss**
58
✂️.....are the **most common** cause of **medication** induced **osteoporosis**.
**Glucocorticoids**
➡️ Inhibits bone formation and increases bone resorption
59
What is the **diagnostic test** and **criteria for osteoporosis**⁉️
**DEXA scan** (Dual-Energy X-ray Absorptiometry)
➡️ T-score ≤ -2.5 at spine or hip
60
Which **medications** are known to cause **osteoporosis**, though less commonly than glucocorticoids⁉️
⚠️ **Heparin**
⚠️ **Lithium**
⚠️ **Omeprazole** (chronic use)
⚠️ **Barbiturates**
61
What are the **most common sites of fracture** in osteoporosis⁉️
📍 **Vertebrae**
📍 **Hip** (femoral neck)
📍 **Distal radius** (Colles fracture)
61
What is the **most appropriate first-line treatment** for severe hypercalcemia due to malignancy⁉️
✅ **IV normal saline** (aggressive hydration)
🧠 Hypercalcemia causes volume depletion → worsens renal function
➡️ Hydration restores renal perfusion and promotes calcium excretion
62
When should **furosemide** be added in the management of hypercalcemia⁉️
✅ **After adequate IV hydration**
💡 Loop diuretics help promote calciuresis, but only after fluid repletion
⛔ Avoid early use — worsens dehydration
62
What is the role of **bisphosphonates** (e.g., alendronate) in hypercalcemia⁉️
✅ **Chronic treatment of malignancy-associated hypercalcemia**
⚠️ Delayed onset (2–4 days)
➡️ **Not** suitable for acute management
62
What are **additional treatments** for severe **hypercalcemia if hydration is not sufficient**⁉️
🔹 **Calcitonin** → rapid but short-acting
🔹 **Bisphosphonates** → intermediate onset
🔹 **Denosumab** → if refractory or bisphosphonates contraindicated
🔹 **Dialysis** → in patients with severe renal failure
62
A patient with **hyperthyroidism**,developed confusion, tachycardia, and fever is most likely experiencing what condition⁉️
✅ **Thyroid storm** (thyrotoxic crisis)
🧠 Life-threatening complication of untreated or triggered hyperthyroidism
⚠️ Precipitating factors: infection, trauma, DKA, surgery, stroke
62
What are the classic **clinical** features of **thyroid storm**⁉️
🚨 **Altered mental status**
🚨 **Fever**
🚨 **Tachycardia**
🚨 **GI symptoms:** vomiting, diarrhea
💡 May progress to heart failure or death if untreated
63
What is the **treatment** protocol for **thyroid storm**⁉️
🔹 **Antithyroid drugs:** propylthiouracil (PTU) or methimazole
🔹 **Beta-blocker:** propranolol (symptom control, ↓ T4→T3 conversion)
🔹 **Steroids:** hydrocortisone or dexamethasone
🔹 **Iodine solution** (e.g., iopanoic acid) after PTU
🔹 **Supportive care:** fluids, cooling blankets, oxygen
🔹 **Antibiotics** if infection is a trigger
64
How is **Graves’ disease** related to thyroid storm⁉️
💡 Graves’ disease is a **common cause** of hyperthyroidism
⚠️ Thyroid storm is an acute, severe exacerbation of hyperthyroidism
➡️ Can occur in poorly controlled Graves’ disease
64
What is the most appropriate **first-line treatment** for a newly diagnosed patient with type 2 diabetes mellitus and A1C of 7%⁉️
✅ **Metformin**
🧠 First-line agent for type 2 DM with proven efficacy, safety, and weight neutrality
65
What is the **mechanism of action** of metformin⁉️
✅ Decreases **hepatic gluconeogenesis**
✅ Improves **peripheral glucose uptake via AMP-activated protein kinase** (AMPK) activation
➡️ No risk of hypoglycemia
66
What are the **major benefits** and **side effects** of metformin⁉️
✅ **Benefits:**
* Lowers A1C by 1–2%
* Mild weight loss
* Improves lipid profile
* Reduces microvascular complications
✅**Side effects:**
* GI upset (nausea, diarrhea)
* Vitamin B12 deficiency
* Rare lactic acidosis
67
Why are **sulfonylureas and pioglitazone** **not** preferred as first-line therapy in a patient recently diagnosed with type 2 diabetes⁉️
⛔ **Sulfonylureas** → risk of hypoglycemia
⛔ **Pioglitazone** → causes weight gain, less effective A1C reduction
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