Pathophysiology

Thirst, hunger and dehydration

obesity, not enough exercise, old age

beta-cells malfunction and hyperglycemia, increased glucose output in the liver

Insulin resistance

lower blood glucose levels, because increased insulin sensitivity due to exercise

At old age due to high glucose levels, usually because blood test for other disease/by chance

1: no insulin production because beta-cells are degraded

2: beta-cells are "exhausted" because of reduced insulin sensitivity

Usually in type 1 diabetes, Hyperglycemia -> lypolysis (increased free fatty acids and uses ketoacids to generate energy, despite of abundance of glucose)

Acidosis forms and dehydration cintiniues to get rid of acids -> osmolarity increases --> (and all over again...)

rapid destruction of pancreatic beta-cells that produce insulin. Mots of the time immune mediated (detection of antibodies possible).
Genetic causes or viral (much less common)

Elevation in blood glucose (hyperglycemia)
Breakdown of body fats and proteins (lipolysis) -> Ketoacidosis develops  (liver converts fatty acids into ketones)

 

Appear sudden. 
Excessive urination (Polyuria) -> Kidney not able to filter glucose
Excessive thirst (Polydipsia) -> Risen Glucose levels cause osmotic dehydration of cells
Excessive hunger (Polyphagia) -> cellular starvation (weightloss)

blurred vision, fatigue
 

Majority of cases (90%). Strong genetic component, Overweight and too little exercise

insulin resistance and increased glucose production in liver.
Have a high or normal insulin level, but decreased sensitivity disables/decreases "use" of it

Often exists for years without detection
Elevated glucose levels
 

Constellation of abnormalities including obesity, high levels of plasma triglycerides, hypertension, systemic inflammation, macrovascular diseases

(Combination of diabetes type 2, high blood pressure and obesity)

Insulin resistance but also other metabolic abnormalities

obesity -> type 2 diabetes (Hyperglycemia) thus insulin resistance
Increased adipose tissue challenges vascular perfusion -> hypoxia (too litle O2), necrosis (irreversible cell injury)
Necrosisi leads to chronic inflammation in adipose tissue -> inadequate response to insulin

Centralor upper body obesity, hypertrophic, elevated glucose levels, insulin resistance, hypertension and atheroclerosis (build up of fat/colesterol in ateries)

Only hormone to lower blood glucose level
Produced in beta cells of pancreas
Inhibits glycogen and fat breakdown and gluconeogenesis by promoting glucose uptake into cells
Targets, fat, muscle and liver cells  mainly
Increases protein synthesis (inhibits breakdown)

Produced by alpha cells in pancreas.
Glucagon travels to liver and initiates glycogen breakdwon into glucose (Glycogenolysis) -> increase blood glucose
increases transport of amino acids into liver

Hormone that acts in the islets of lagerhans to decrese secretion of insulin and glucagon
Triggered by food ingestion, glucose blood level, fatty acids and amino acids
Decreases gastrointestinal motility and slows food absorption -> increase time of nutrient availability

Increase insulin release and decrease glucagon release (also called incretin effect)

GLP1 is a glucagon like peptide (that does what above written)

Metabolic effect which inculdes increased cellular protein synthesis, release fatty acids
Insulin inhibits secretion of Growth hormone
Hypersecretion can lead to glucose intolerance

Helps maintaining blood glucose levels during preiods of stress -> stimulates glycogenolysis in liver
inhibits insulin release
Affects adipose tissues by lipolysis -> increase availability of fatty acids for energy

Type 2 diabetes in children with obesity
Etiology: Genetic disease limits ability to produce insulin (but not completely absent), sensitivity is normal
Patophysiology: Mutation that leads to impaired insulin secretion
Clinical manifestation: Polyuria (pee), Polydipsia (thirst)

Diabetic ketoacidosis is a complication of (mostly) type 1 diabetes

Three major metabolic derangements: Hyperglycemia, ketosis and metabolic acidosis

Insulin defficiency -> Hyperglycemia -> osmotic dehydration of cells
Insulin defficiency -> lipolysis that produces free fatty acids and glycerol -> travel to liver and result in ketones -> leads to ketosis and metabolic acidosis (excess of keto acids)
 

Polyuria, Polydipsia, Nauesa, vomitting, and fatigue -> can progress to comma
fruity smel of breath
Hypotension and tachycardia 

Occurs in people treated with insulin -> too much insulin, failure to eat,...

1. Caused by altered brain functions: headaches, difficulty in problem solving, altered, vision, seizures

2. Related to activation of autonomic nervous system: hunger, anxiety, tachycardia, sweating constriction of blood vessels -> cool and clammy skin

Neoplasia is an abnormal mass of tissue, with uncoordinated and exceeding growth relative to normal tissues. It does not serve any useful purpose and is not in response to a stimulus

Tumors usually have the suffix -oma

They are classified into benign (good) and malignant (bad)

Adenoma and Osteoma
Carcinoma and Sarcoma

Cell characteristics: Benign are well differentiated (resemble normal cells)
Rate of growth: Benign grows slow and progressive
Manner of growth: Benign expand but stay local
Capacity to invade and metastasize: Benign do not
Potential for causing death: Benign only if interfere with vital functions due to location

Well differentiated cells that resemble normal tissue
Slow progression and rate of growth
Lost ability to supress proliferation but not differentiation
Grow by expansion but do not invade ot metastasize
Usually not deadly unless location affects vital functions (e.g. pressure on blood vessels/nerves)
Might cause abnormal hormone production -> alterations in body functions
 

Undifferentiated cells and rapid growth (the more undifferentiated cells the faster)
Uncoordinated grow due to lack of control of proliferation and differentiation
Grow by invasion and metastasize to distant sites
Might supress blood vessels and outgrow their blood supply -> ischemia
Secrete hormones,cytokines,enzymes or toxins and induce inflammatory response