Personal life @subuhihasan - Tumblr Blog

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No matter how honest you're with other people but cunning clever people never stop being cleverly cunning because they are born this way.

Life experiences ⛓️‍💥

32trbl

bymins_

diewithasmile-e

chand-azaad-ghadiyan

My roommate is obsessed with me.

Am I this good? 😂😅

subuhihasan

A bitch : Jinn bhuth ki tarah pure time mere upar nazar rakhti hai.......!

icaseybaybee

I think I'm the most stupid on this planet ever I do believe people so easily without even understanding simple thing koi mujhse sach Kyun bolega mein kanha Ki maharani hon

Me and my tab against this world...!

Thyroid function and blood sugar levels are closely linked, having an underactive thyroid (hypothyroidism) can increase your risk of low blood sugar (hypoglycemia).

Hypothyroidism slows down your body's metabolism, which can lead to hypoglycemia through several mechanisms....!

Reduced glucose production: The liver produces less glucose (gluconeogenesis & glycogenolysis)

Slower insulin clearance : Insulin stays in the bloodstream longer than usual...!

Slower digestion : The body absorbs glucose from food more slowly due to delayed gastric emptying....!

Medical case reports illustrate this link ; for example, a 32-year-old woman was hospitalized with recurrent hypoglycemia (blood sugar as low as 20 mg/dL) and was eventually diagnosed with severe hypothyroidism. Her symptoms resolved after starting thyroid hormone replacement.

Similarly, a 73-year-old man with type 2 diabetes experienced recurrent hypoglycemia that didn't respond to his usual diabetes management, He was also diagnosed with overt hypothyroidism, and his blood sugar stabilized after treatment.

Important Note: This link is strongest for hypothyroidism, while rare, severe hyperthyroidism (overactive thyroid) can also lead to hypoglycemia under extreme conditions, such as severe illness or starvation....!

Biochemistry : Eating my carbs knowing they will undergo glycolysis, Krebs cycle, ETC & oxidative phosphorylation to form some ATPS....! 🍟🍔

Physiology : The Renin-Angiotensin-Aldosterone System (RAAS) Pathway......!

1. Stimulus : The cascade is initiated in response to physiological stress, specifically : low Blood Pressure (Hypotension), Low Sodium (Hyponatremia).....!

2. Renal Phase - Enzyme Release Renin from (Juxtaglomerular apparatus)

3. Hepatic Phase (Substrate Production) Liver releases a precursor protein cld Angiotensinogen into the bloodstream

4. First Conversion Step : Renin acts on Angiotensinogen and produce Angiotensin I (an inactive decapeptide)

5. Pulmonary Phase (Second Conversion) Lungs (specifically the pulmonary vascular endothelium) Enzyme : ACE (Angiotensin-Converting Enzyme) It cleaves Angiotensin I and produce Angiotensin II (an active octapeptide) this is the primary effector hormone of the system.

6. Systemic Effects of Angiotensin II : Once formed, Angiotensin II acts on multiple target organs to restore blood pressure and volume

a) Vasoconstriction (systemic arteriolar constriction) Result : Increased systemic vascular resistance (SVR) → Increased Blood Pressure b) Adrenal Glands : Stimulates the release of Aldosterone....Aldosterone promotes renal Salt & Water Retention (increases sodium reabsorption and potassium excretion) → Increased Blood Volume!

Brain : Stimulates ADH (Antidiuretic Hormone) Secretion from posterior pituitary and increase Thirst! Result : ADH increases water reabsorption in the kidney's collecting ducts, and thirst drives fluid intake → Increased Blood Volume....!

To control BP perks...! Note : ACE Inhibitors (e.g. Lisinopril) block the conversion of Angiotensin I to II in the lungs

ARBs (e.g. Losartan) block Angiotensin II receptors....!

Both classes are first-line treatments for hypertension and heart failure because they break this cycle of vasoconstriction and fluid retention...!

se-a09

julaibib

Low imaan isn’t hypocrisy. It’s human. Even the best of people experience it. The solution is not guilt or silence. It’s dua. That’s why the Prophet ﷺ taught us to ask Allah to strengthen our faith. Because imaan is a gift, and gifts are asked for.

Itne imtehaan phir bhi mere dil mein jaan abhi baki hai....kyunki karbala jane ka armaan abhi baki hai......!❤️

ACS (Acute Coronary Syndrome) Clinical Management Pathway!

Initial Presentation

Patient : Presents with Acute Chest Pain

Immediate Diagnostic Step : Perform a 12-Lead ECG (must be completed within 10 minutes of arrival)

BRANCH A : ST Elevation Present? (YES)

Diagnosis : STEMI (ST-Elevation Myocardial Infarction) Immediate Medical Management (MONA Protocol)

M - Morphine (for pain relief)

O - Oxygen (if hypoxic)

N - Nitroglycerine (sublingual or IV)

A - Aspirin (antiplatelet)

Adjunctive Pharmacotherapy :

Antiplatelets : (e.g, Clopidogrel, Ticagrelor, or Prasugrel) Anticoagulants : (e.g. Heparin or Enoxaparin)

Reperfusion Strategy : Immediate Reperfusion

First-Line Strategy : Primary PCI (Percutaneous Coronary Intervention) is the preferred gold-standard treatment

Alternative (Fallback): Thrombolysis (fibrinolytic therapy - alteplase reteplase and tenecteplase 30 - 50 mg) is indicated only if PCI is unavailable or cannot be performed within the recommended time window (90min to 12hrs)

BRANCH B : ST Elevation Present? (NO)

Diagnostic step : Check Serum Troponin levels

Scenario 1 : Elevated Troponin ↑

Diagnosis : NSTEMI (Non-ST-Elevation Myocardial Infarction)

Management Protocol :

Antiplatelets, Anticoagulants

Procedural Strategy :

1. Risk Stratification : Assess patient risk scores (e.g, GRACE or TIMI score) to determine urgency!

2. Early Invasive Strategy : Proceed to Angiography ± PCI (Percutaneous Coronary Intervention)

Scenario 2: Normal Troponin

Diagnosis: UNSTABLE ANGINA (UA)

Note : Both NSTEMI and Unstable Angina are classified as Non-ST-Elevation ACS (NSTE-ACS)