Cholecystokinin is secreted from duodenum, jejunum and ileum. Cholecystokinin has several functions. It stimulates contraction of gall bladder, activate secretin, increase secretion of Enterokinase, inhibited gastric motility and increase intestinal motility.
Gastrin is a hormone important for acid secretion in the stomach. Gastrin secreted mainly from the G cells in the stomach. Other than that TG cells in stomach, duodenum and jejunum, Islets of fetal pancreases, anterior pituitary and brain also secrete gastrin.
Main action is secretion of gastric juice. It also increase gastric motility, promotes growth of gastric mucosa and stimulates release of pancreatic hormones.
There are 3 types of contractions. Peristalsis, segmental contractions and tonic contractions. Peristalsis move food forwards toward to large intestine. Segmental contraction helps to mix food and expose food to mucosa. Tonic contraction are prolong isolated contraction in the segments. Segmental and tonic contractions are slow when the presence of food.
Phosphorylcreatine is converted to creatinine. Creatinine excretion is relatively constant and that make creatinine is good indicator of renal function. Creatinine is freely filtered in the glomeruli and nether reabsorb nor secrete in the tubules.
Creatinine Kinase
Present in cytoplasm.
3 Types – CK1 MM - Skeletal
CK2 MB - Cardiac
CK3 BB - Brain
Size of enzyme Size of infarct
CK2 MB – Start rise in 4-6 hours.
– Peak in 24 hours.
– Back to normal in 48 hours.
– More specific than total CK.
Action-
Creatinine Creatinine Phosphate
Creatinine Kinase
ATP ADP
Lactate Dehydrogenase
Present in cytoplasm – Heart , Liver, Kidney
Found highest concenration in Heart.
Start to rise - 12-18 hours.
Peak at - 48-72 hours.
Return normal – 6-8 days.
Non specific.
Action- Lactate Pyruvate
Lactate Dehydrogenase
NADH + H+ NAD+
Aspartate Transaminase
Seen in Heart, Liver & RBC.
Starts to rise – 3-8 hours.
Peak at – 24 hours.
Return to normal – 3-6 days.
Action – Aspartate Oxaloacetate
α – KG Glutamate
Troponin
Complex of 3 protein sub units.
1. Troponin C
2. Troponin I
3. Troponin T
Two types of cardiac troponins.
Troponin I & Troponin T
Normal person has a negligible amount.
So even small infarct can be markedly
increased.
More sensitive & cardiac specific than CK2MB.
Cardiac Troponin T (cTnT)
Start increasing within few hours.
Reaches peak in about 14 hours.
2nd peak level is seen between 3-5 days.
Level remains elevated for up to 7 days.
Cardiac Troponin I (cTnI)
The peak value achieved – similar to cTnT.
Specific marker of myocardial injury – in
renal or multi organ damage.
Glycogen Phosphorylase BB (GPBB)
Key enzyme involved in glycogenolysis.
Has greater discriminatory ability than
CKMB, cTnT, & Myoglobin within the 1st
four hours of onset of pain.
Myoglobin
O2 binding protein. (cardiac & skeletal
muscles.)
Released earlier than CK from damaged cell.
Rise above reference level 1 hour after MI.
Peak activity – 4-12 hours.
Lacked laboratory & clinical acceptance.
Aldosterone is important for sodium reabsorption in several places in the body. In the collecting ducts of the kidney, adlosterone facilitated sodium reabsorption in the P cells. It helps to open Na+ channels.
Anti diuretic hormone
This is one important hormone for water conservation in the body. ADH increase reabsorption of water in the collecting duct of kidney. It helps to activate V2 receptors in the protein water channels – aquaporins-2. ADH cause rapid translation to luminal membrane.
ANP increase sodium excretion in the body and acts mainly in the kidney. ANP produced from atrium. ANP increase glomerular filtration rate by dilating afferent arterioles and relaxing mesangial cells. It also acts on renal tubules and inhabits sodium reabsorption.
Other than it’s main effect on kidney, ANP increases capillary permeability and relax vascular smooth muscles in arterioles and veins.
Forceful expulsion of gastrointestinal content is vomiting. There should be antiperistalsis movement and content should move opposite direction.
Vomiting results from squeezing of abdominal muscle with sudden opening of oesophageal sphincters.
Vomiting is regulated by vomiting centre located in the brain. There are some sequent of event. First take deep breathe and rising of hyoid bone at larynx to pull open the upper oesophageal sphincter. Then closing of glottis and letting soft palate to close nostrils. Abdominal muscles and diaphragm contact and pressure cause opening of lower oesophageal sphincter.
Ischemic syndromes may result,
(Depending on the rate of the development of the arterial narrowing.)
1. Angina Pectoris.
2. Myocardial Infarction. (MI)
– most important form.
3. Chronic Ischemic Heart Disease.
4. Sudden Cardiac Death.
MI is the most common cause of death in
industrialized nations.
MI almost always occurs in patients with
coronary atheroma.
Clinical diagnosis of acute MI based on
three sets of data.
I. Symptoms.
II. ECG changes.
III. Rise/Fall in cardiac enzyme.
I. Symptoms
Severe chest pain similar in character to angina.(20% of patients have no pain.)
II. ECG changes
ST elevation & T wave inversion.
III. Rise / Fall in cardiac enzymes
Necrotic cardiac tissue release several enzymes as
follows.
1. Creatinine Kinase. (CK)
2. Lactate Dehydrogenase. (LDH)
3. Aspartate Amino Transferase. (AST)(SGOT)
4. Cardiac specific Troponin.
I. Troponin I
II. Troponin T
5. Glycogen Phosphorylase –BB (GPBB)